Ca2+ effluxes from the sarcoplasmic reticulum vesicles of frog muscle: effects of cyclopiazonic acid and thapsigargin

Du, Guo-Guang; Ashley, Christopher; Lea, T. J.

doi:10.1016/s0143-4160(96)90041-x

Cited by 21 publications

(21 citation statements)

References 25 publications

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“…However, DTT is a sulfhydryl-reducing agent that is not specific for any particular protein (5), and we have shown that DTT can alter the effects of skeletal muscle ischemia on measurements of SR Ca 2ϩ -ATPase activity (39). In HL-60 cells, it was concluded that the apparent Ca 2ϩ release induced by AgNO 3 was mainly due to inhibition of the Ca 2ϩ pump with increased permeability for Ca 2ϩ (10). This mechanism cannot explain the rapid AgNO 3 -induced Ca 2ϩ release response observed in the present study.…”

Section: Discussionmentioning

confidence: 98%

Silver ions induce Ca²⁺release from the SR in vitro by acting on the Ca²⁺release channel and the Ca²⁺pump

Tupling

Green

2002

Journal of Applied Physiology

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release channel (CRC), causing the channel to open. To further examine the effects of AgNO 3 on the CRC and the Ca 2ϩ -ATPase, Ca 2ϩ release was measured in muscle homogenates prepared from rat hindlimb muscle using indo 1. Cyclopiazonic acid (CPA) and ruthenium red (RR) were used to inhibit the Ca 2ϩ -ATPase and block the CRC, respectively, before inducing Ca 2ϩ release with both AgNO3 and 4-chlorom-cresol (4-CMC), a releasing agent specific for the CRC. With AgNO3 and CPA, the early rapid rate of release (phase 1) was increased (P Ͻ 0.05) by 42% (314 Ϯ 5 vs. 446 Ϯ 39 mol ⅐ g protein Ϫ1 ⅐ min Ϫ1 ), whereas the slower, more prolonged rate of release (phase 2) was decreased (P Ͻ 0.05) by 72% (267 Ϯ 39 vs. 74 Ϯ 7.7 mol ⅐ g protein Ϫ1 ⅐ min Ϫ1 ). RR, in combination with AgNO3, had no effect on phase 1 (P Ͼ 0.05) (314 Ϯ 51 vs. 334 Ϯ 43 mol ⅐ g protein Ϫ1 ⅐ min Ϫ1 ) and decreased phase 2 (P Ͻ 0.05) by 65% (245 Ϯ 34 vs. 105 Ϯ 8.2 mol ⅐ g protein Ϫ1 ⅐ min Ϫ1 ). With 4-CMC, CPA had no effect (P Ͼ 0.05) on either phase 1 or 2. With addition of RR, phase 1 was reduced (P Ͻ 0.05) by 59% (2,468 Ϯ 279 vs.

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Section: Discussionmentioning

confidence: 98%

Silver ions induce Ca²⁺release from the SR in vitro by acting on the Ca²⁺release channel and the Ca²⁺pump

Tupling

Green

2002

Journal of Applied Physiology

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“…Alternatively, the leakage could occur through a modified type of ryanodine receptor, given that it has been reported that Ca¥ leaks out of mammalian skeletal muscle SR through a pathway that is insensitive to both ryanodine and RR and that this pathway can be converted back to the normal ryanodine-sensitive state by the sponge extract, bastadin-5 (Pessah et al 1997). A third possibility is that the leak occurs via some quite different pathway, such as through the SR CaATPase; such Ca¥ leakage has been observed in frog SR vesicles and was not blocked by Mg¥, ryanodine or RR (Du et al 1996;. Importantly, the Ca¥ leakage rate was increased approximately 3-fold after high [Ca¥] treatment ( Fig.…”

Section: Discussion Caffeine Assay Of Ca¥ Contentmentioning

confidence: 99%

High intracellular [Ca²⁺] alters sarcoplasmic reticulum function in skinned skeletal muscle fibres of the rat

Lamb

Cellini

1999

The Journal of Physiology

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1. The effect on sarcoplasmic reticulum (SR) function of exposure to high intracellular [Ca¥] was studied in mechanically skinned fibres from the extensor digitorum longus muscle of the rat, using caffeine to assay the SR Ca¥ content. 2. A 15 s exposure to 50 ìÒ Ca¥ irreversibly reduced the ability of the SR to loadÏretain Ca¥ and completely abolished depolarization-induced Ca¥ release, whereas a 90 s exposure to 10 ìÒ Ca¥ had no detectable effect on either function. The reduction in net SR Ca¥ uptake: (a) was near-maximal with treatment at 50 ìÒ Ca¥, (b) was unrelated to voltage-sensor function, and (c) persisted unchanged for > 20 min. The reduction was primarily due to a threefold increase in leakage of Ca¥ out of the SR. This increased leakage was not substantially blocked by the presence of 10 mÒ Mg¥ or 2 ìÒ Ruthenium Red. 3. The adverse effect on SR function of exposure to high [Ca¥] could also be observed by the reduction in the ability of the SR to maintain a low [Ca¥] within the skinned fibre in the face of elevated [Ca¥] METHODS Isolation of skinned fibresLong-Evans hooded rats (Rattus norvegicus) aged 14 to 20 weeks were anaesthetized by halothane (2 % vÏv) and killed by asphyxiation in accordance with guidelines of the La Trobe University Animal Ethics Committee. As described previously (Lamb & Stephenson, 1994), both extensor digitorum longus muscles were then removed and placed in paraffin oil and kept cool on ice. Single muscle fibres were dissected free at one end from the muscle and mechanically skinned. The skinned fibre segment was mounted onto a force transducer (AME875, SensoNor, Horten, Norway), and stretched to 120% of its resting length. The fibre was then placed into a 2 ml Perspex bath containing a potassium or sodium 1,6-diaminohexane-N,N,N' ,N'-tetraacetic acid (HDTA) solution to equilibrate before being stimulated by rapid substitution of an appropriate solution. All experiments were performed at room temperature (23 ± 2°C). SolutionsAll chemicals were obtained from Sigma unless stated otherwise. The make-up of the solutions used in the different parts of the experiments is set out below. All solutions had a pH of 7·10 ± 0·01 and an osmolality of 295 ± 5 mosmol kg¢, and unless stated otherwise had 1 mÒ free Mg¥ and 8 mÒ total ATP. Free [Ca¥] at ü 0·1 ìÒ was verified with a Ca¥-sensitive electrode (Orion, Cambridge, MA, USA) . Leak solution. K-HDTA solution with 2 mÒ total EGTA (pCa > 8), but otherwise similar to pre-equilibration solution. Used to allow Ca¥ leakage from the SR in the absence of Ca¥ uptake. Additional matching solutions were also made with 10 mÒ free Mg¥ (22·7 mÒ total magnesium) or with all K¤ replaced with Na¤ (for chronic T-system depolarization).Contractile apparatus experiments Relaxing solution. Potassium solution with 50 mÒ EGTA (pCa > 9), which is similar to the polarizing solution with all HDTA replaced with EGTA (see Stephenson & Williams, 1981).Maximum-activation solution. Same as Relaxing solution but with 50 mÒ CaEGTA (pCa 4·5). Referred to as 'M...

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“…Ca 2ϩ is probably released from intracellular stores, through endogenous leaks that become apparent following Ca 2ϩ pump inhibition (26,27). In untransfected HEK-293 cells, 1 M thapsigargin caused a slow phase of Ca 2ϩ release (n ϭ 3, data not shown).…”

Section: Caffeine-induced Ca 2ϩ Release From Hek-293 Cells Transfectementioning

confidence: 94%

Characterization of Recombinant Rabbit Cardiac and Skeletal Muscle Ca2+ Release Channels (Ryanodine Receptors) with a Novel [3H]Ryanodine Binding Assay

Du¹,

Imredy²,

MacLennan

1998

Journal of Biological Chemistry

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Ca2+ effluxes from the sarcoplasmic reticulum vesicles of frog muscle: effects of cyclopiazonic acid and thapsigargin

Cited by 21 publications

References 25 publications

Silver ions induce Ca²⁺release from the SR in vitro by acting on the Ca²⁺release channel and the Ca²⁺pump

Silver ions induce Ca²⁺release from the SR in vitro by acting on the Ca²⁺release channel and the Ca²⁺pump

High intracellular [Ca²⁺] alters sarcoplasmic reticulum function in skinned skeletal muscle fibres of the rat

Characterization of Recombinant Rabbit Cardiac and Skeletal Muscle Ca2+ Release Channels (Ryanodine Receptors) with a Novel [3H]Ryanodine Binding Assay

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Ca2+ effluxes from the sarcoplasmic reticulum vesicles of frog muscle: effects of cyclopiazonic acid and thapsigargin

Cited by 21 publications

References 25 publications

Silver ions induce Ca2+release from the SR in vitro by acting on the Ca2+release channel and the Ca2+pump

Silver ions induce Ca2+release from the SR in vitro by acting on the Ca2+release channel and the Ca2+pump

High intracellular [Ca2+] alters sarcoplasmic reticulum function in skinned skeletal muscle fibres of the rat

Characterization of Recombinant Rabbit Cardiac and Skeletal Muscle Ca2+ Release Channels (Ryanodine Receptors) with a Novel [3H]Ryanodine Binding Assay

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Product

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Silver ions induce Ca²⁺release from the SR in vitro by acting on the Ca²⁺release channel and the Ca²⁺pump

Silver ions induce Ca²⁺release from the SR in vitro by acting on the Ca²⁺release channel and the Ca²⁺pump

High intracellular [Ca²⁺] alters sarcoplasmic reticulum function in skinned skeletal muscle fibres of the rat