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  • Ca2+ release
  • 2005-2009  (1)
  • 1980-1984  (2)
  • 1
    Publication Date: 2022-05-25
    Description: First published online as a Review in Advance on October 24, 2005. (Some corrections may occur before final publication online and in print)
    Description: Author Posting. © Annual Reviews, 2005. This article is posted here by permission of Annual Reviews for personal use, not for redistribution. The definitive version was published in Annual Review of Physiology 68 (2006): 22.1-22.29, doi:10.1146/annurev.physiol.68.040104.105418.
    Description: Superfast muscles of vertebrates power sound production. The fastest, the swimbladder muscle of toadfish, generates mechanical power at frequencies in excess of 200 Hz. To operate at these frequencies, the speed of relaxation has had to increase approximately 50-fold. This increase is accomplished by modifications of three kinetic traits: (a) a fast calcium transient due to extremely high concentration of sarcoplasmic reticulum (SR)-Ca2+ pumps and parvalbumin, (b) fast off-rate of Ca2+ from troponin C due to an alteration in troponin, and (c) fast cross-bridge detachment rate constant (g, 50 times faster than that in rabbit fast-twitch muscle) due to an alteration in myosin. Although these three modifications permit swimbladder muscle to generate mechanical work at high frequencies (where locomotor muscles cannot), it comes with a cost: The high g causes a large reduction in attached force-generating cross-bridges, making the swimbladder incapable of powering low-frequency locomotory movements. Hence the locomotory and sound-producing muscles have mutually exclusive designs.
    Description: This work was made possible by support from NIH grants AR38404 and AR46125 as well as the University of Pennsylvania Research Foundation.
    Keywords: Parvalbumin ; Ca2+ release ; Ca2+ uptake ; Cross-bridges ; Adaptation ; Sound production ; Whitman Center
    Repository Name: Woods Hole Open Access Server
    Type: Article
    Format: 567086 bytes
    Format: application/pdf
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 66 (1982), S. 193-201 
    ISSN: 1432-1424
    Keywords: sarcoplasmic reticulum ; Ca2+ release ; excitation-contraction coupling ; muscular contraction ; valinomycin ; ruthenium red
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Ca2+-induced Ca2+ release at the terminal cisternae of skeletal sarcoplasmic reticulum was demonstrated using heavy sarcoplasmic reticulum vesicles. Ca2+ release was observed at 10 μm Ca2+ in the presence of 1.25mm free Mg2+ and was sensitive to low concentrations of ruthenium red and was partially inhibited by valinomycin. These results suggest that the Ca2+-induced Ca2+ release is electrogenic and that an inside negative membrane potential created by the Ca2+ flux opens a second channel that releases Ca2+. Results in support of this formulation were obtained by applying a Cl− gradient or K+ gradient to sarcoplasmic reticulum vesicles to initiate Ca2+ release. Based on experiments the following hypothesis for the excitation-contraction coupling of skeletal muscle was formulated. On excitation, small amounts of Ca2+ enter from the transverse tubule and interact with a Ca2+ receptor at the terminal cisternae and cause Ca2+ release (Ca2+-induced Ca2+ release). This Ca2+ flux generates an inside negative membrane potential which opens voltage-gated Ca2+ channels (membrane potential-dependent Ca2+ release) in amounts sufficient for contraction.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 76 (1983), S. 165-171 
    ISSN: 1432-1424
    Keywords: sarcoplasmic reticulum ; Ca2+-ATPase ; Ca2+ transport ; Ca2+ release ; osmotic swelling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The ATP-dependent accumulation of Ca2+ by sarcoplasmic reticulum vesicles at 37° C reaches a peak after approximately 100 sec. The Ca2+-loading level then declines until a steady-state level is reached which is 20% less than the peak value. This spontaneous release of Ca2+ is enhanced by inclusion of maleate in the Ca2+ uptake medium. Increasing the extravesicular osmolarity by the addition of sucrose to the Ca2+ uptake medium prevents spontaneous Ca2+ release and increases the steady-state Ca2+-loading capacity of sarcoplasmic reticulum vesicles. Swelling of sarcoplasmic reticulum vesicles during Ca2+ uptake in medium containing sucrose is indicated by changes in the light-scattering intensity. These experiments indicate that the capacity of sarcoplasmic reticulum vesicles to accumulate Ca2+ is limited by the osmotic gradient generated by the increase in intravesicular Ca2+. Swelling of sarcoplasmic reticulum vesicles during Ca2+ uptake causes spontaneous Ca2+ release.
    Type of Medium: Electronic Resource
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