Voltage-gated and calcium-gated calcium release during depolarization of skeletal muscle fibers

Jacquemond, Vincent; Csernoch, László; Klein, Michael G.; Schneider, Martin F.

doi:10.1016/s0006-3495(91)82120-8

Cited by 95 publications

(145 citation statements)

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“…The present results together with the recent work of Jacquemond et al (1991) are evidence of a calcium-induced mechanism contributing to physiological calcium release. This, together with the effects of released calcium on the voltage sensor, either causing or modifying the charge movement component Qy Jong, Pape & Chandler, 1992), brings to two the number of positive feedback processes apparently at work in the control of calcium release.…”

Section: Tetracaine Effects On Charge Movementsupporting

confidence: 82%

“…The pharmacology of this process observed in skinned fibres, isolated triads and reconstituted channels, argues strongly in this direction. Most importantly, Jacquemond, Csernoch, Klein & Schneider (1991) showed that intracellular injection of the fast calcium buffer bis(O-aminophenoxy)ethane-NNN',N'-tetraacetic acid (BAPTA) in frog cut fibres abolishes the peak of calcium release and spares the noninactivating component. The effects of BAPTA are remarkably similar to those of tetracaine reported in this paper and both sets of experiments paint a consistent picture of two release processes, separately controlled by voltage and Ca2 .…”

Section: Two Distinct Pathways Of Calcium Releasementioning

confidence: 99%

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Differential effects of tetracaine on two kinetic components of calcium release in frog skeletal muscle fibres.

Pizarro

Csernoch

Uribe

et al. 1992

The Journal of Physiology

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SUMMARY1. Intramembrane charge movements and changes in intracellular calcium concentration were recorded simultaneously in voltage clamped cut skeletal muscle fibres of the frog in the presence and absence of tetracaine.2. Extracellular application of 20 /IM tetracaine reduced the increase in myoplasmic [Ca2"]. The effect on the underlying calcium release flux from the sarcoplasmic reticulum was to suppress the peak of the release while sparing the steady level attained at the end of 100 ms clamp depolarizations.3. While the peak of the release flux at corresponding voltages was reduced by 62 o after the addition of tetracaine, the rate of inactivation was the same when the pulses elicited release fluxes of similar amplitude.4. Higher concentrations of tetracaine, 0-2 mm, abolished the calcium signal in stretched fibres whereas in slack fibres this concentration left a non-inactivating calcium release flux.5. Lowering the extracellular pH antagonized the effect of the drug both on charge movements and on calcium signals. The permanently charged analogue tetracaine methobromide lacked effects on excitation-contraction coupling.6. These results imply that the two kinetic components of calcium release flux have very different tetracaine sensitivities. They are also consistent with an intracellular site of action of the drug at low concentration. Taken together they strongly suggest that the inactivating and non-inactivating components of calcium release correspond to different pathways: one that inactivates, is sensitive to tetracaine and is controlled by calcium, and another that does not inactivate, is much less sensitive to tetracaine and is directly controlled by voltage.

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Section: Tetracaine Effects On Charge Movementsupporting

confidence: 82%

Section: Two Distinct Pathways Of Calcium Releasementioning

confidence: 99%

Differential effects of tetracaine on two kinetic components of calcium release in frog skeletal muscle fibres.

Pizarro

Csernoch

Uribe

et al. 1992

The Journal of Physiology

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“…Our laboratory previously showed that partial depolarization of MHN fibers with KCl increased their [Ca 2ϩ ] i and resulted in increased caffeine response (27). BAPTA is a high-affinity Ca 2ϩ chelator (46, 47) that has been used in several previous studies to reduce [Ca] i in adult skeletal muscle fibers (3,19). As an intracellular Ca 2ϩ buffer, BAPTA has several important advantages over other Ca 2ϩ chelators, because it is practically insensitive to intracellular pH changes, has a greater selectivity for Ca 2ϩ over Mg 2ϩ , is faster than EDTA and EGTA at taking up and releasing Ca 2ϩ , and its dissociation constant is 110 nM (46,47).…”

Section: Discussionmentioning

confidence: 99%

Enhanced response to caffeine and 4-chloro-m-cresol in malignant hyperthermia-susceptible muscle is related in part to chronically elevated resting [Ca²⁺]_i

López¹,

Linares²,

Pessah³

et al. 2005

American Journal of Physiology-Cell Physiology

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[Ca 2ϩ ]i, and reduced the amount of Ca 2ϩ release associated with exposure to any given concentration of caffeine or 4-CmC to MHN levels. These results suggest that the differences in the response of MHS skeletal myoballs to caffeine and 4-CmC may be mediated at least in part by the chronic high resting [Ca 2ϩ ]i levels in these cells. calcium homeostasis; 1,2-bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid MALIGNANT HYPERTHERMIA (MH) is a potentially fatal pharmacogenetic myopathy of humans and several large mammals, including swine, dog, and horse. It can be induced by volatile anesthetics and/or depolarizing muscle relaxants (1, 33, 37). While in swine susceptibility to the syndrome has been associated with a single point mutation (Arg615Cys) in the Ca 2ϩ release channel at the sarcoplasmic reticulum (ryanodine receptor 1, RyR1) (13, 32), in humans at least 42 MH mutations have been identified at 34 different RyR1 residues and two MH mutations at one residue in the skeletal dihydropyridine receptor (DHPR) (21,33,37 (17,26). In addition, it was previously shown that skeletal muscle from MHS individuals and animals have a lower pharmacological threshold and an exaggerated response at submaximal concentrations of caffeine (22, 45) and 4-chloro-m-cresol (4-CmC) (44, 48) than do those with MH-nonsusceptible (MHN) muscle. This enhanced sensitivity is widely used as part of the clinical diagnosis of MH susceptibility in humans and has been confirmed experimentally in swine (16,21). The molecular and cellular basis for heightened sensitivity to pharmacological agents in MHS has remained unclear (33, 37). Evidence of chronically elevated resting [Ca 2ϩ ] i has been presented on the basis of direct measurements with Ca 2ϩ -selective electrodes in isolated human and swine skeletal muscle fibers (28, 30). However, the extent to which high [Ca 2ϩ ] i contributes to sensitizing responses to caffeine and 4-CmC is not known.The purpose of the present study was to address the question of whether the enhanced intracellular Ca 2ϩ release at submaximal concentrations of caffeine and 4-CmC (44,45,48) in MHS cells is related to chronic elevation in resting [Ca 2ϩ ] i in affected muscle cells. To do so, resting [Ca 2ϩ ] i of MHS myoballs was decreased nearly to MHN levels by loading them with the Ca 2ϩ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid (BAPTA) and then reexamining the responses to caffeine and 4-CmC. Our results suggest that the enhanced intracellular Ca 2ϩ release at submaximal concentrations of caffeine and 4-CmC was closely associated with the high resting [Ca 2ϩ ] i observed in these cells. MATERIALS AND METHODSMuscle cell preparations. Muscle biopsies were obtained from the hindlimb muscles of newborn (4 -8 days) Yorkshire (MHN; n ϭ 4) and Poland China (MHS; n ϭ 5) swine. Susceptibility to MH was determined using polymerase chain reaction genotyping as previously described (33, 37). Hindlimb muscle was removed while the animals were anesthetized with the nontriggering age...

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“…The possibility that the early peak of Ca 2ϩ release during voltage-clamp depolarization is composed mainly of CICR, whereas the later quasi-steady level is the result of direct DHPR activation has been repeatedly considered since an early study by Jacquemond et al (112), who reported that Ca buffer specifically inhibits the early peak. Shirokova et al (231) has found that amphibian skeletal muscles, which have equal amounts of RyR␤ and RyR␣, show a much more prominent early peak than do mammalian muscles, which have only a small amount of RyR3, and suggested that Ca 2ϩ released from DHPR-activated RyR␣ channels may activate the CICR of RyR␤ to cause the more-prominent early peak in amphibian muscles (231).…”

Section: B Early Peak Of Voltage-activated Ca 2؉ Release and Cicrmentioning

confidence: 99%

Calcium-Induced Calcium Release in Skeletal Muscle

Endo¹

2009

Physiological Reviews

261

223

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Calcium-induced calcium release (CICR) was first discovered in skeletal muscle. CICR is defined as Ca2+ release by the action of Ca2+ alone without the simultaneous action of other activating processes. CICR is biphasically dependent on Ca2+ concentration; is inhibited by Mg2+, procaine, and tetracaine; and is potentiated by ATP, other adenine compounds, and caffeine. With depolarization of the sarcoplasmic reticulum (SR), a potential change of the SR membrane in which the luminal side becomes more negative, CICR is activated for several seconds and is then inactivated. All three types of ryanodine receptors (RyRs) show CICR activity. At least one RyR, RyR1, also shows non-CICR Ca2+ release, such as that triggered by the t-tubule voltage sensor, by clofibric acid, and by SR depolarization. Maximum rates of CICR, at the optimal Ca2+ concentration in the presence of physiological levels of ATP and Mg2+ determined in skinned fibers and fragmented SR, are much lower than the rate of physiological Ca2+ release. The primary event of physiological Ca2+ release, the Ca2+ spark, is the simultaneous opening of multiple channels, the coordinating mechanism of which does not appear to be CICR because of the low probability of CICR opening under physiological conditions. The coordination may require Ca2+, but in that case, some other stimulus or stimuli must be provided simultaneously, which is not CICR by definition. Thus CICR does not appear to contribute significantly to physiological Ca2+ release. On the other hand, CICR appears to play a key role in caffeine contracture and malignant hyperthermia. The potentiation of voltage-activated Ca2+ release by caffeine, however, does not seem to occur through secondary CICR, although the site where caffeine potentiates voltage-activated Ca2+ release might be the same site where caffeine potentiates CICR.

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Voltage-gated and calcium-gated calcium release during depolarization of skeletal muscle fibers

Cited by 95 publications

References 36 publications

Differential effects of tetracaine on two kinetic components of calcium release in frog skeletal muscle fibres.

Differential effects of tetracaine on two kinetic components of calcium release in frog skeletal muscle fibres.

Enhanced response to caffeine and 4-chloro-m-cresol in malignant hyperthermia-susceptible muscle is related in part to chronically elevated resting [Ca²⁺]_i

Calcium-Induced Calcium Release in Skeletal Muscle

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Voltage-gated and calcium-gated calcium release during depolarization of skeletal muscle fibers

Cited by 95 publications

References 36 publications

Differential effects of tetracaine on two kinetic components of calcium release in frog skeletal muscle fibres.

Differential effects of tetracaine on two kinetic components of calcium release in frog skeletal muscle fibres.

Enhanced response to caffeine and 4-chloro-m-cresol in malignant hyperthermia-susceptible muscle is related in part to chronically elevated resting [Ca2+]i

Calcium-Induced Calcium Release in Skeletal Muscle

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Enhanced response to caffeine and 4-chloro-m-cresol in malignant hyperthermia-susceptible muscle is related in part to chronically elevated resting [Ca²⁺]_i