Ca2+ Release Channel of Sarcoplasmic Reticulum: Characterization of the Regulatory Sites

  • Gerhard Meissner
Part of the Series of the Centro de Estudios Científicos de Santiago book series (SCEC)


This chapter focuses on an unresolved aspect of muscle function, namely, how does sarcoplasmic reticulum (SR) release calcium ions, thereby causing muscle to contract? A schematic drawing of a small segment of a muscle cell is depicted in the upper part of Fig. 1. Two key structures in excitation-contraction coupling—the surface membrane, composed of the sarcolemma and transverse (T-)system, and the SR—are shown. SR is an intracellular membrane system whose main function is to regulate muscle contraction and relaxation by releasing and taking up again the released Ca2+. Rapid release from skeletal muscle SR is triggered by a surface membrane potential that is thought to be communicated to SR at specialized areas where the SR comes in close contact with the T-tubule, and protein bridges (“feet”) are present which span the gap between the two membrane systems. However, how calcium ions are released from SR has remained an enigma(1,2) (also see Chapter 22, this book). One hypothesis is that T-tubule depolarization increases in the junctional gap the concentration of a chemical messenger such as Ca2+, which then opens a Ca2+ -channel in the SR membrane. Another popular hypothesis suggests that the feet are in direct contact with a voltage-sensing molecule in the T-tubule membrane. During T-tubule depolarization the feet undergo a conformational change which regulates the opening of the SR Ca2+-channels.


Sarcoplasmic Reticulum Release Channel Adenine Nucleotide Efflux Rate Release Vesicle 
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Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Gerhard Meissner
    • 1
  1. 1.Departments of Biochemistry and Physiology, School of MedicineUniversity of North CarolinaChapel HillUSA

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