Functional aspects of calcium transport in sarcoplasmic reticulum vesicles derived from frog skeletal muscle treated with saponin

Fanò, Giorgio; Belia, Silvia; Fulle, Stefania; Angelella, P.; Panara, Fausto; Marsili, Valeria; Pascolini, Rita

doi:10.1007/bf01758428

Cited by 19 publications

(6 citation statements)

References 18 publications

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“…This treatment permeabilizes the sarcolemmal and T-tubules membranes, leaving the sarcoplasmic reticulum intact [7,29]. Then, in these skinned fibres, the mechanisms of sarcoplasmic reticulum Ca 2+ loading and release could be studied [8].…”

Section: Solutionmentioning

confidence: 99%

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Talon¹,

Huchet-Cadiou²,

Léoty³

2000

Pflügers Arch - Eur J Physiol

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Previous reports have shown that cooling striated muscles induces contractile responses that are related to Ca2+ release from the sarcoplasmic reticulum. However, the effect of cooling has generally been studied in the presence of pharmacological agents that potentiate rapid cooling-induced contractures. The present study shows that in saponin-skinned rat skeletal muscle preparations, a drop in temperature from 22 degrees C to 2 degrees C per se induces a contracture which relaxes on return to 22 degrees C. In fast-twitch fibres, rapid cooling-induced contractures are fully blocked by ryanodine, an inhibitor of ryanodine receptors. By contrast, in slow-twitch fibres, ryanodine partially inhibits the rapid cooling-induced contractile response, leaving a residual tension that dissipates after application of inositol 1,4,5-trisphosphate (InsP3). At low concentrations, heparin, an inhibitor of InsP3 receptors, decreases rapid cooling-induced contractures in both types of muscle. The present results suggest that in skeletal muscle, rapid cooling-induced contractures are due to both ryanodine-sensitive and InsP3-sensitive Ca2+ release from the sarcoplasmic reticulum.

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Section: Solutionmentioning

confidence: 99%

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Talon¹,

Huchet-Cadiou²,

Léoty³

2000

Pflügers Arch - Eur J Physiol

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“…The skinned fibres were then washed several times in relaxing solution without detergent. This treatment permeabilises the sarcolemmal and Ttubule membranes, leaving the sarcoplasmic reticulum intact and functional [10]. With this preparation, it is possible to load the sarcoplasmic reticulum with different levels of Ca 2+ and then to release the latter with pharmacological tools such as caffeine, an activator of the ryanodine receptors [20].…”

Section: Tension/pca Relationshipsmentioning

confidence: 99%

Sarcoplasmic reticulum function in slow- and fast-twitch skeletal muscles from mdx mice

Divet

Huchet-Cadiou

2002

Pfl�gers Archiv European Journal of Physiology

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The aim of the present study was to establish whether alterations in sarcoplasmic reticulum function are involved in the abnormal Ca(2+) homeostasis of skeletal muscle in mice with muscular dystrophy ( mdx). The properties of the sarcoplasmic reticulum and contractile proteins of fast- and slow-twitch muscles were therefore investigated in chemically skinned fibres isolated from the extensor digitorum longus (EDL) and soleus muscles of normal (C57BL/10) and mdx mice at 4 and 11 weeks of development. Sarcoplasmic reticulum Ca(2+) uptake, estimated by the Ca(2+) release following exposure to caffeine, was significantly slower in mdx mice, while the maximal Ca(2+) quantity did not differ in either type of skeletal muscle at either stage of development. In 4-week-old mice spontaneous sarcoplasmic reticulum Ca(2+) leakage was observed in EDL and soleus fibres and this was more pronounced in mdx mice. In addition, the maximal Ca(2+)-activated tension was smaller in mdx than in normal fibres, while the Ca(2+) sensitivity of the contractile apparatus was not significantly different. These results indicate that mdx hindlimb muscles are affected differently by the disease process and suggest that a reduced ability of the Ca(2+)-ATPase to load Ca(2+) and a leaky sarcoplasmic reticulum membrane may be involved in the altered intracellular Ca(2+) homeostasis.

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“…This treatment preserves the ability of the SR to accumulate and release Ca 2ϩ (Fano et al, 1989). After skinning, fibers were transferred and mounted in a manner similar to that of Huchet and Léoty (1993).…”

Section: Methodsmentioning

confidence: 99%

Methyl Jasmonate-Induced Stimulation of Sarcoplasmic Reticulum Ca²⁺-ATPase Affects Contractile Responses in Rat Slow-Twitch Skeletal Muscle

Joumaa

Bouhlel²,

Même³

et al. 2002

J Pharmacol Exp Ther

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The purpose of this study was to determine whether methyl jasmonate, a stimulator of Ca 2ϩ -adenosine triphosphatase (ATPase) activity of the purified ATPase from fast-twitch skeletal muscle, could affect contractile responses in small bundles of rat isolated slow-twitch (soleus) fibers. In saponin-skinned fibers, sarcoplasmic reticulum (SR) Ca 2ϩ loading was performed in pCa 7.0 solution. The amount of Ca 2ϩ taken up was monitored by use of the amplitude of contraction following application of 10 mM caffeine. Results indicate that the increased loading rate in the presence of methyl jasmonate is likely due to stimulation of the SR Ca 2ϩ -ATPase. In Triton-skinned fibers, the myofibrillar Ca 2ϩ sensitivity was not changed by methyl jasmonate (50 -200 M). In intact fibers, the amplitude and the time constant of relaxation of twitch and potassium contracture were reversibly reduced after 2 min of application of methyl jasmonate at a concentration of up to 125 M. At higher concentrations (Ͼ150 M), effects were not reversible. In the presence of methyl jasmonate (100 M), the relationship between the amplitude of potassium contractures and the membrane potential shifted to more positive potentials, whereas the steady-state inactivation curve was unchanged. These observations suggest that methyl jasmonate has no effect on voltage sensors. Taken together, our results show that methyl jasmonate is a potent, reversible, and specific stimulator of the SR Ca 2ϩ pump in slow-twitch skeletal muscle and is an extremely valuable pharmacological tool for improving relaxation and studying calcium-signaling questions.

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Functional aspects of calcium transport in sarcoplasmic reticulum vesicles derived from frog skeletal muscle treated with saponin

Cited by 19 publications

References 18 publications

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Sarcoplasmic reticulum function in slow- and fast-twitch skeletal muscles from mdx mice

Methyl Jasmonate-Induced Stimulation of Sarcoplasmic Reticulum Ca²⁺-ATPase Affects Contractile Responses in Rat Slow-Twitch Skeletal Muscle

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Functional aspects of calcium transport in sarcoplasmic reticulum vesicles derived from frog skeletal muscle treated with saponin

Cited by 19 publications

References 18 publications

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Rapid cooling-induced contractures in rat skinned skeletal muscle fibres originate from sarcoplasmic reticulum Ca2+ release through ryanodine and inositol trisphosphate receptors

Sarcoplasmic reticulum function in slow- and fast-twitch skeletal muscles from mdx mice

Methyl Jasmonate-Induced Stimulation of Sarcoplasmic Reticulum Ca2+-ATPase Affects Contractile Responses in Rat Slow-Twitch Skeletal Muscle

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Product

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Methyl Jasmonate-Induced Stimulation of Sarcoplasmic Reticulum Ca²⁺-ATPase Affects Contractile Responses in Rat Slow-Twitch Skeletal Muscle