Abstract
Contraction and relaxation of skeletal muscle is controlled by two membrane systems, the transverse tubular and the longitudinal system (sarcoplasmic reticulum). Under physiological conditions, electrical depolarization of the T-tubular membrane triggers a rapid release of Ca2+ ions from the sarcoplasmic reticulum (SR), leading to an increase in the intracellular free Ca2+ concentration and finally to a contraction of muscle fibre. The communication between the two membrane systems occurs in specialized areas where large protein structures, termed feet or bridges (Franzini-Armstrong, 1986), span the narrow gap between the transverse tubules and the SR. Although the mechanism of signal transmission remains to be elucidated [for recent reviews see Rios & Pizzaro, 1988; Caswell & Brandt, 1989; Fleischer & Inui, 1989], there is now good evidence that SR Ca2+ release is mediated via a high con-ductant ligand-gated Ca2+ release channel which serves as the receptor for the plant alkaloid ryanodine and has been shown to be identical with the feet protein [Fleischer & Inui, 1989; Lai & Meissner, 1989; Takeshima et al., 1990].
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© 1991 Springer-Verlag Berlin Heidelberg
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Herrmann-Frank, A. (1991). Regulation of Ca2+ Release from Sarcoplasmic Reticulum of Skeletal Muscle by an Endogenous Substance. In: Rüegg, J.C. (eds) Peptides as Probes in Muscle Research. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76409-7_13
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DOI: https://doi.org/10.1007/978-3-642-76409-7_13
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-76411-0
Online ISBN: 978-3-642-76409-7
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