Structure of the Calcium Release Channel of Skeletal Muscle Sarcoplasmic Reticulum and Its Regulation by Calcium

  • F. Anthony Lai
  • Gerhard Meissner
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 269)


Skeletal muscle contraction is initiated by an action potential-induced depolarization of the muscle plasma membrane. This electrical excitation originates at the neuromuscular synapse and spreads rapidly into the transverse tubule (T-) system of membrane infoldings, which extend inward from the surface membrane to surround each myofibril. In an incompletely understood process termed excitation-contraction coupling (Somlyo, 1985), T-system depolarization somehow triggers the rapid release of a large Ca2+ pool stored within the intracellular membrane system, sarcoplasmic reticulum (SR), thus providing an elevated free Ca2+ concentration that results in muscle contraction (Ebashi, 1976; Endo, 1977). The signal which induces opening of the SR Ca2+ release channels is believed to be transmitted at specialized junctions where the T-system and SR membranes become closely apposed to form a narrow 12 nm gap. Large protein structures projecting from the SR membrane span this junctional gap to provide apparent continuity between the T-system and SR, and have previously been defined morphologically and termed either feet (Franzini-Armstrong, 1970), bridges (Somlyo, 1979), pillars (Eisenberg and Eisenberg, 1982) or spanning proteins (Caswell and Brunschwig, 1984). Biochemical and morphological analysis of SR fragmented by homogenization of muscle tissue has shown that both Ca2+ release activity and the feet structures are enriched in “heavy” SR vesicles, a subcellular microsomal fraction derived from the junctional SR (Nagasaki and Kasai, 1983; Meissner, 1984; Ferguson et al., 1984; Saito et al., 1984; Ikemoto et al., 1985; Meissner et al., 1986). Study of the Ca2+ release channel activity using isolated heavy SR vesicles has been approached by applying two complementary techniques; macroscopic 45Ca2+ flux from passively loaded vesicles, and microscopic Ca2+ currents through single channels incorporated into planar lipid bilayers. Vesicle 45Ca2+ flux studies have shown that the SR Ca2+ release channel can be activated by micromolar Ca2+ or millimolar adenine nucleotides to give enhanced release rates, but could be optimally activated only by the combined presence of Ca2+ and adenine nucleotides to give maximal release rates with first-order rate constants of 30–100s-1 (Meissner et al., 1986).


Sarcoplasmic Reticulum Release Channel Ryanodine Receptor Planar Lipid Bilayer Sarcoplasmic Reticulum Membrane 
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Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • F. Anthony Lai
    • 1
  • Gerhard Meissner
    • 1
  1. 1.Departments of Biochemistry and PhysiologyUniversity of North Carolina, School of MedicineChapel HillUSA

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