Regulation of Ca2+ Release from Sarcoplasmic Reticulum of Skeletal Muscle by an Endogenous Substance
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].
KeywordsHPLC Filtration Acetonitrile Glycine Serine
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