Kinetic separation of charge movement components in intact frog skeletal muscle.

Huang, Christopher L.‐H.

doi:10.1113/jphysiol.1994.sp020445

Cited by 14 publications

(53 citation statements)

References 34 publications

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“…The charging currents decreased in amplitude, particularly with the larger shifts in holding potential from -90 mV. Similar values of maximum charge, Q~ax(VH), close to 20 nC p~F 1, and similar inactivation functions in agreement with those reported on earlier occasions (Huang, 1994b), were obtained under all conditions, whether RyR antagonists were present or absent. Thus, the total steady-state charge or the corresponding charge movements were all not affected by small holding potential shifts between -90 and -70 mV, but charge steeply declined with larger changes toward -40 or -50 mV.…”

Section: Fig 4 Compares Results In Control Fibers (Open Squares)supporting

confidence: 78%

“…Thus, all the entries confirm similar reduced values of maximum charge, Q~ax, and similarly shallow voltage dependences (k ~ 14-16 mV) distinct from those shown by the overall charge in Table I. All these features fulfill expectations for q~ charge in the presence of extracellular gluconate (Chen and Hui, 1991;Huang, 1994b). Least-squares minimizations of maximum charge, ~,~x 20 transition voltage, VH*, and slope factor, k (given as means + SEM), in a single Boltzmann inactivation function given by Q-z0(VH) = ~ax 20 1 -1/{1 + exp[-(VH--VH*)/k]}} for n fibers in each case.…”

Section: The Modified Q~ Isoform Retains Its Steady-state Pharmacologsupporting

confidence: 68%

“…A step depolarization in a fully polarized intact fiber first elicits a rapidly rising q~ signal that then decays approximately indistinguishable from the remaining capacity transient, with larger depolarizations that nevertheless transferred increased steady-state charge (Huang, 1994b). Thus, their kinetic, steady-state, and pharmacological properties closely paralleled the steep voltage dependence shown by the release of intracellularly stored Ca 2+ (Huang, 1981a(Huang, , 1982(Huang, , 1993Hui, 1983;Vergara and Caputo, 1983;Chandler, 1990, 1991).…”

Section: Introductionmentioning

confidence: 85%

“…This provided optimal conditions for the measurement of absolute quantifies of steady-state charge and for the discrimination of q~ charge with which comparisons could be drawn with other findings obtained in similar experimental solutions (Huang, 1994a(Huang, , 1994b. They demonstrated that RyR modification by ryanodine and daunorubicin (see Discussion; for a review see Meissner, 1994) altered q~ charge movements in a manner compatible with a reciprocal coupling between RyRs and the DHPRs in turn responsible for the observed charge transfers (Huang, 1990).…”

Section: Introductionmentioning

confidence: 85%

“…It also provided records that emphasized the distinction between q~ and q~ charge movement (cf. Chen and Hui, 1991;Huang 1994aHuang , 1994bsee Introduction). Finally, the substantial replacement of external Ca 2+ by Mg 2+ suppressed Ca 2+ currents, and the inclusion of 3,4-diaminopyridine as well as tetraethylammonium ions suppressed K + currents.…”

Section: Effective Conditions For Antagonist Actionmentioning

confidence: 99%

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Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

Huang

1996

The Journal of General Physiology

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The effects of the ryanodine receptor (RyR) antagonists ryanodine and daunorubicin on the kinetic and steady-state properties of intramembrane charge were investigated in intact voltage-clamped frog skeletal muscle fibers under conditions that minimized timedependent ionic currents. A hypothesis that RyR gating is allosterically coupled to configurational changes in dihydropyridine receptors (DHPRs) would predict that such interactions are reciprocal and that RyR modification should influence intramembrane charge. Both agents indeed modified the time course of charging transients at 100-200-p.M concentrations. They independently abolished the delayed charging phases shown by q~ currents, even in fibers held at fully polarized, -90-mV holding potentials; such waveforms are especially prominent in extracellular solutions containing gluconate. Charge movements consistently became exponential decays to stable baselines in the absence of intervening inward or other time-dependent currents. The steady-state charge transfers nevertheless remained equal through the ON and the OFF parts of test voltage steps. The charge-voltage function, Q(VT), shifted by ~+ 10 mV, particularly through those test potentials at which delayed q~ currents normally took place but retained steepness factors (k ~ 8.0 to 10.6 mV) that indicated persistent, steeply voltage-dependent q~ contributions. Furthermore, both RyR antagonists preserved the total charge, and its variation with holding potential, Qma~(VH), which also retained similarly high voltage sensitivities (k ~ 7.0 to 9.0 mV). RyR antagonists also preserved the separate identities of qv and qa species, whether defined by their steady-state voltage dependence or inactivation or pharmacological properties. Thus, tetracaine (2 mM) reduced the available steady-state charge movement and gave shallow Q(VT) (k --~ 14 to 16 mV) and Qma~(VH) (k 14 to 17 mV) curves characteristic of q~ charge. These features persisted with exposure to test agent. Finally, q~ charge movements showed steep voltage dependences with both activation (k ~ 4.0 to 6.5 mV) and inactivation characteristics (k ~ 4.3 to 6.6 mV) distinct from those shown by the remaining q~ charge, whether isolated through differential tetracaine sensitivities, or the full approximation of charge-voltage data to the sum of two Boltzmann distributions. RyR modification thus specifically alters qx kinetics while preserving the separate identities of steady-state qf~ and q~ charge. These findings permit a mechanism by which transverse tubular voltage provides the primary driving force for configurafional changes in DHPRs, which might produce q~ charge movement. However, they attribute its kinetic complexities to the reciprocal allosteric coupling by which DHPR voltage sensors and RyR-Ca 2 § release channels might interact even though these receptors reside in electrically distinct membranes. RyR modification then would still permit tubular voltage change to drive net q~ charge transfer but would transform its complex waveforms into s...

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Section: Fig 4 Compares Results In Control Fibers (Open Squares)supporting

confidence: 78%

Section: The Modified Q~ Isoform Retains Its Steady-state Pharmacologsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 85%

Section: Effective Conditions For Antagonist Actionmentioning

confidence: 99%

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Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

Huang

1996

The Journal of General Physiology

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FPL-64176 alters both charge movement and Ca 2+ release properties in amphibian muscle fibres

Chawla

Huang

2004

Pfl�gers Archiv European Journal of Physiology

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A number of recent reports have suggested that ryanodine receptor (RyR)-Ca2+ release channels are gated by tubular depolarization in skeletal muscle through their direct coupling to intramembrane dihydropyridine receptor (DHPR)-voltage sensors. The qgama charge movement, which is inhibited by DHPR antagonists, is often regarded as the electrical signature for the voltage sensing process, yet pharmacological modifications of the RyR produce reciprocal upstream kinetic effects on an otherwise conserved qgamma charge. This study investigates the effect of DHPR-specific agonists upon intramembrane charge and the release of intracellularly stored Ca2+. We empirically demonstrate kinetic effects of FPL-64176 upon charge movements that closely resemble the consequences of previous interventions directed instead at the RyR. Increases in extracellular FPL-64176 concentration from 10 to 40 microM converted delayed qgamma transients to monotonic decays indistinguishable from the exponential qbeta current component. Yet total steady-state intramembrane charge and the steepness of its dependence upon test potential closely resembled previous reports from untreated fibres. These changes accompanied an appearance of transient cytosolic [Ca2+] elevations in confocal line-scans in fluo-3-loaded fibres studied in 10mM K+ and 40, but not 10 microM, FPL-64176 that resembled elementary Ca2+ release events ('sparks'). Pharmacological manipulations of the DHPR whose effects on intramembrane charge resembled those from manoeuvres directed at the RyR can thus produce downstream effects upon Ca2+ release.

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Effects of membrane depolarization and changes in extracellular [K+] on the Ca2+ transients of fast skeletal muscle fibers. Implications for muscle fatigue

Quiñonez

González

Morgado-Valle

et al. 2010

J Muscle Res Cell Motil

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Repetitive activation of skeletal muscle fibers leads to a reduced transmembrane K+ gradient. The resulting membrane depolarization has been proposed to play a major role in the onset of muscle fatigue. Nevertheless, raising the extracellular K+ (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ {\text{K}}_{\text{o}}^{ + } $$\end{document}) concentration (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ [ {\text{K}}^{ + } ]_{\text{o}} $$\end{document}) to 10 mM potentiates twitch force of rested amphibian and mammalian fibers. We used a double Vaseline gap method to simultaneously record action potentials (AP) and Ca2+ transients from rested frog fibers activated by single and tetanic stimulation (10 pulses, 100 Hz) at various \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ [ {\text{K}}^{ + } ]_{\text{o}} $$\end{document} and membrane potentials. Depolarization resulting from current injection or raised \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ [ {\text{K}}^{ + } ]_{\text{o}} $$\end{document} produced an increase in the resting [Ca2+]. Ca2+ transients elicited by single stimulation were potentiated by depolarization from −80 to −60 mV but markedly depressed by further depolarization. Potentiation was inversely correlated with a reduction in the amplitude, overshoot and duration of APs. Similar effects were found for the Ca2+ transients elicited by the first pulse of 100 Hz trains. Depression or block of Ca2+ transient in response to the 2nd to 10th pulses of 100 Hz trains was observed at smaller depolarizations as compared to that seen when using single stimulation. Changes in Ca2+ transients along the trains were associated with impaired or abortive APs. Raising \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ [ {\text{K}}^{ + } ]_{\text{o}} $$\end{document} to 10 mM potentiated Ca2+ transients elicited by single and tetanic stimulation, while raising \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{...

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Kinetic separation of charge movement components in intact frog skeletal muscle.

Cited by 14 publications

References 34 publications

Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

FPL-64176 alters both charge movement and Ca 2+ release properties in amphibian muscle fibres

Effects of membrane depolarization and changes in extracellular [K+] on the Ca2+ transients of fast skeletal muscle fibers. Implications for muscle fatigue

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