Calcium release from sarcoplasmic reticulum of normal and dystrophic mice

Volpe, Pompeo; Mrak, Robert E.; Costello, Brian; Fleischer, Sidney

doi:10.1016/0005-2736(84)90010-5

Cited by 20 publications

(18 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Movement of ions across the SR membrane to counter this negative potential has been implicated in the efficient operation of VICR in skeletal muscle and CICR in cardiac muscle [10][11][12][13][14][15]. Although channels selective for monovalent cations have been reported in SR membrane [10,14,[16][17][18], until recently no gene has been identified that encodes an ER/SR localized cation-selective channel.…”

Section: Introductionmentioning

confidence: 99%

Immuno-proteomic approach to excitation–contraction coupling in skeletal and cardiac muscle: Molecular insights revealed by the mitsugumins

Weisleder

Takeshima

2008

Cell Calcium

View full text Add to dashboard Cite

A comprehensive understanding of excitation-contraction (E-C) coupling in skeletal and cardiac muscle requires that all the major components of the Ca 2+ release machinery be resolved. We utilized a unique immuno-proteomic approach to generate a monoclonal antibody library that targets proteins localized to the skeletal muscle triad junction, which provides a structural context to allow efficient E-C coupling. Screening of this library has identified several mitsugumins (MG); proteins that can be localized to the triad junction in mammalian skeletal muscle. Many of these proteins, including MG29 and junctophilin, are important components in maintaining the structural integrity of the triad junction. Other triad proteins, such as calumin, play a more direct role in regulation of muscle Ca 2+ homeostasis. We have recently identified a family of trimeric intracellular cation-selective (TRIC) channels that allow for K + movement into the endoplasmic or sarcoplasmic reticulum to counter a portion of the transient negative charge produced by Ca 2+ release into the cytosol. Further study of TRIC channel function and other novel mitsugumins will increase our understanding of E-C coupling and Ca 2+ homoeostasis in muscle physiology and pathophysiology.

show abstract

Section: Introductionmentioning

confidence: 99%

Immuno-proteomic approach to excitation–contraction coupling in skeletal and cardiac muscle: Molecular insights revealed by the mitsugumins

Weisleder

Takeshima

2008

Cell Calcium

View full text Add to dashboard Cite

show abstract

“…However, in frog atrial trabecula this triggering action of caffeine can be delayed by local anaesthetics that are known to antagonize the actions of caffeine, by hypertonic solutions and by rapid cooling, probably by blocking the release of Ca2l from the SR (Feinstein, 1963;Chapman & Ellis, 1973;Chapman & Miller, 1974;Chapman, 1977;Volpe, Palade, Costello, Mitchell & Fleischer, 1983;Chamberlain et al 1984). This delay means that if a frog atrial trabecula is exposed to ryanodine, followed by caffeine in the presence of tetracaine (2 mM), the inhibition of the caffeine contracture prevents its triggering action, so that any following caffeine contracture is normal, but as it will now trigger the action of the alkaloid, all subsequent caffeine or rapid cooling contractures are inhibited (Fig.…”

Section: Discussionmentioning

confidence: 99%

The effect of ryanodine on the contraction of isolated frog atrial trabeculae is triggered by caffeine

Tunstall

Ra²

1994

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYRyanodine is without effect on the contraction of frog atrial muscle when applied alone. However, if agents which bring about Ca2+ release from the sarcoplasmic reticulum (SR), e.g. caffeine, hypertonic fluid or rapid cooling, are applied together with or up to 1 h after exposure to ryanodine, subsequent effects upon contraction are evident. These include a complete inhibition of the contractures evoked by caffeine, rapid cooling or hypertonic solutions applied in Na+-deficient media and a shift in the relationship between [Ca2+]. and the strength of the heart beat to a higher [Ca2+] The contractures evoked by Na+ withdrawal are unaffected. These results have been interpreted as an action of ryanodine to maintain the open state of the SR Ca2+-release channels, thereby inhibiting Ca2+ accumulation by the SR. In this respect the response of the frog heart resembles mammalian heart, but differs in that this action is not triggered by the normal heart beat. These results add support to the notion that, although contraction can be activated in frog atrial muscle by release of Ca2+ from the SR, it is not a major source of Ca2+ during the normal heart beat.

show abstract

“…As Volpe et al (1983) showed, spontaneous calcium release in light sarcoplasmic reticulum is not inhibited by ruthenium red and therefore cannot include a rutheniumred-sensitive calcium channel (today known as ryanodine receptor) as opposed to observations in heavy sarcoplasmic reticulum.…”

Section: Discussionmentioning

confidence: 99%

Caffeine‐induced calcium oscillations in heavy‐sarcoplasmic‐reticulum vesicles from rabbit skeletal muscle

Wyskovsky¹

1994

European Journal of Biochemistry

View full text Add to dashboard Cite

Heavy-sarcoplasmic-reticulum vesicles from rabbit skeletal muscle show not only caffeine-induced calcium release in a medium allowing active calcium loading, but also oscillations in calcium concentration under appropriate conditions. The xanthine derivatives 7-isobutyl-1-methylxanthine and theophylline also induce oscillations under the same conditions. Calcium-releasing substances with other chemical structures such as adenosine nucleotides or calmodulin antagonists do not induce this effect. With the help of specific inhibitors such as ruthenium red, neomycin or magnesium it was demonstrated that the oscillation mechanism involves the ryanodine receptor/calcium channel. When ATP was substituted by GTP or ITP no oscillations occurred after caffeine application. The subsequent application of ATP, but not of adenosine 5'-[y-thio]triphosphate or adenosine 5'-[jS,y-methylene]triphosphate activated the oscillating mechanism, showing ATP to be an essential component of the oscillating system. We investigated the influence of the experimental conditions by altering the caffeine and ATP concentrations, calcium load, pH and ionic strength amongst other parameters. Potassium and anion channels are not involved in calcium oscillations of heavy sarcoplasmic reticulum, nor are the oscillations dependent on membrane potential.

show abstract

Calcium release from sarcoplasmic reticulum of normal and dystrophic mice

Cited by 20 publications

References 31 publications

Immuno-proteomic approach to excitation–contraction coupling in skeletal and cardiac muscle: Molecular insights revealed by the mitsugumins

Immuno-proteomic approach to excitation–contraction coupling in skeletal and cardiac muscle: Molecular insights revealed by the mitsugumins

The effect of ryanodine on the contraction of isolated frog atrial trabeculae is triggered by caffeine

Caffeine‐induced calcium oscillations in heavy‐sarcoplasmic‐reticulum vesicles from rabbit skeletal muscle

Contact Info

Product

Resources

About