Role of extracellular metal cations in the potential dependence of force inactivation in skeletal muscle fibres

Schnier, A.; Lüttgau, Hans-Christoph; Melzer, Werner

doi:10.1007/bf00141553

Cited by 12 publications

(12 citation statements)

References 19 publications

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“…The reduction or removal of extracellular Ca 2+ has effects on sensor charge and associated Ca 2+ currents similar to those of sustained depolarization, dihydropyridines, and other inactivation-promoting drugs in both frog Ca V 1.1 ( Ríos and Pizarro, 1991 ; Schnier et al, 1993 ; Melzer et al, 1995 ) and mammalian Ca V 1.2 ( Field et al, 1988 ; Shirokov et al, 1993 ). In agreement with the early findings, we now demonstrate that the Q ( V ) distribution present in depolarized cells does not change in 0 [Ca 2+ ] e ( Fig.…”

Section: Discussionmentioning

confidence: 99%

The voltage sensor of excitation–contraction coupling in mammals: Inactivation and interaction with Ca2+

Ferreira

Pequera

Manno

et al. 2017

Journal of General Physiology

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Section: Discussionmentioning

confidence: 99%

The voltage sensor of excitation–contraction coupling in mammals: Inactivation and interaction with Ca2+

Ferreira

Pequera

Manno

et al. 2017

Journal of General Physiology

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“…Numerous studies have further demonstrated that this spontaneous relaxation results from an inactivation process that promotes closure of SR Ca 2+ release channels in a voltage- and time-dependent manner. As we explored in the present study, time and voltage dependence of the inactivation process have been investigated by examining the effects of conditioning pulses on voltage-induced Ca 2+ or force transients, or indirectly of high K + solutions on K + -induced contractures (Hodgkin and Horowicz, 1960; Lüttgau and Spiecker, 1979; Caputo et al, 1984; Brum et al, 1988; Schnier et al, 1993). These steady-state or double-pulse inactivation protocols revealed that inactivation of Ca 2+ release requires depolarizations lasting seconds or tens of seconds to develop and is associated with immobilization of intramembrane charge movements, suggesting that inactivation of Ca 2+ release channels arises from transition of the voltage sensor that controls its opening into an inactivated state (Chandler et al, 1976; Brum and Rios, 1987).…”

Section: Discussionmentioning

confidence: 99%

Major contribution of sarcoplasmic reticulum Ca2+ depletion during long-lasting activation of skeletal muscle

Robin

Allard

2013

Journal of General Physiology

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Depolarization of skeletal muscle fibers induces sarcoplasmic reticulum (SR) Ca2+ release and contraction that progressively decline while depolarization is maintained. Voltage-dependent inactivation of SR Ca2+ release channels and SR Ca2+ depletion are the two processes proposed to explain the decline of SR Ca2+ release during long-lasting depolarizations. However, the relative contribution of these processes, especially under physiological conditions of activation, is not clearly established. Using Fura-2 and Fluo-5N to monitor cytosolic and SR Ca2+ changes, respectively, in voltage-controlled mouse muscle fibers, we show that 2-min conditioning depolarizations reduce voltage-activated cytosolic Ca2+ signals with a V1/2 of −53 mV but also induce SR Ca2+ depletion that decreased the releasable pool of Ca2+ with the same voltage sensitivity. In contrast, measurement of SR Ca2+ changes indicated that SR Ca2+ release channels were inactivated after SR had been depleted and in response to much higher depolarizations with a V1/2 of −13 mV. In response to trains of action potentials, cytosolic Ca2+ signals decayed with time, whereas SR Ca2+ changes remained stable over 1-min stimulation, demonstrating that SR Ca2+ depletion is exclusively responsible for the decline of SR Ca2+ release under physiological conditions of excitation. These results suggest that previous studies using steady-state inactivation protocols to investigate the voltage dependence of Ca2+ release inactivation in fact probed the voltage dependence of SR Ca2+ depletion, and that SR Ca2+ depletion is the only process that leads to Ca2+ release decline during continuous stimulation of skeletal muscle.

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“…Slow voltage–dependent inactivation of Ca 2+ release has been studied in voltage-clamped adult muscle fibers of the frog both by force measurements and by Ca 2+ measurements (e.g., Caputo and Fernandez, 1979 ; Caputo and Bolanos, 1987 ; Pizarro et al, 1988 ; Schnier et al, 1993 ). In adult mammalian muscle, properties of inactivation have been indirectly assessed by K + depolarization and force measurements ( Chua and Dulhunty, 1988 , 1989 ; Dulhunty, 1991 ), but data on Ca 2+ release flux inactivation in mammalian muscle have not been available until now.…”

Section: Discussionmentioning

confidence: 99%

Altered Inactivation of Ca2+ Current and Ca2+ Release in Mouse Muscle Fibers Deficient in the DHP receptor γ1 subunit

Ursu

Schuhmeier

Freichel

et al. 2004

The Journal of General Physiology

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Functional impacts of the skeletal muscle-specific Ca2+ channel subunit γ1 have previously been studied using coexpression with the cardiac α1C polypeptide in nonmuscle cells and primary-cultured myotubes of γ1-deficient mice. Data from single adult muscle fibers of γ−/− mice are not yet available. In the present study, we performed voltage clamp experiments on enzymatically isolated mature muscle fibers of the m. interosseus obtained from γ+/+ and γ−/− mice. We measured L-type Ca2+ inward currents and intracellular Ca2+ transients during 100-ms step depolarizations from a holding potential of −80 mV. Ratiometric Ca2+ transients were analyzed with a removal model fit approach to calculate the flux of Ca2+ from the sarcoplasmic reticulum. Ca2+ current density, Ca2+ release flux, and the voltage dependence of activation of both Ca2+ current and Ca2+ release were not significantly different. By varying the holding potential and recording Ca2+ current and Ca2+ release flux induced by 100-ms test depolarizations to +20 mV, we studied quasi-steady-state properties of slow voltage–dependent inactivation. For the Ca2+ current, these experiments showed a right-shifted voltage dependence of inactivation. Importantly, we could demonstrate that a very similar shift occurred also in the inactivation curve of Ca2+ release. Voltages of half maximal inactivation were altered by 16 (current) and 14 mV (release), respectively. Muscle fiber bundles, activated by elevated potassium concentration (120 mM), developed about threefold larger contracture force in γ−/− compared with γ+/+. This difference was independent of the presence of extracellular Ca2+ and likely results from the lower sensitivity to voltage-dependent inactivation of Ca2+ release. These results demonstrate a specific alteration of voltage-dependent inactivation of both Ca2+ entry and Ca2+ release by the γ1 subunit of the dihydropyridine receptor in mature muscle fibers of the mouse.

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Role of extracellular metal cations in the potential dependence of force inactivation in skeletal muscle fibres

Cited by 12 publications

References 19 publications

The voltage sensor of excitation–contraction coupling in mammals: Inactivation and interaction with Ca2+

The voltage sensor of excitation–contraction coupling in mammals: Inactivation and interaction with Ca2+

Major contribution of sarcoplasmic reticulum Ca2+ depletion during long-lasting activation of skeletal muscle

Altered Inactivation of Ca2+ Current and Ca2+ Release in Mouse Muscle Fibers Deficient in the DHP receptor γ1 subunit

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