The effect of diameter on the electrical constants of frog skeletal muscle fibres

Hodgkin, A. L.; Nakajima, Shigehiro

doi:10.1113/jphysiol.1972.sp009742

Cited by 193 publications

(170 citation statements)

References 27 publications

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“…It was further possible to assess fiber condition and stability in the intact preparations through computations of length constants, h, internal longitudinal resistances, r~, and membrane resistances of unit fiber length, rm. Calculation of fiber diameters, d, and specific membrane resistances, Rm, assumed an internal sarcoplasmic resistivity,/~, of 391 l-I cm in 2.5 times hypertonic solution at 2~ and a temperature coefficient of 0.73 (Hodgkin and Nakajima, 1972); these calculations were performed for each individual average. In contrast, such values of rm and Rm could not be unambiguously determined in cut fibers studied between Vaseline seals, owing to current shunts heneath the seals .…”

Section: Methodsmentioning

confidence: 99%

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: Methodsmentioning

confidence: 99%

Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

Huang

1996

The Journal of General Physiology

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“…They gave values of the length constant, ~t, internal longitudinal resistance, r~, and membrane resistance of unit fiber length, r m. The fiber diameter, d, and specific membrane resistance, R,,,, were then calculated. This assumed a value of the internal sarcoplasmic resistivity, R i, of 391 ohm.cm in 2.5 times hypertonic solution at 2°C, with a Ql0 of 0.73 (Hodgkin and Nakajima, 1972). The membrane current through unit area of fiber surface, Im(t ), was computed as:…”

Section: Methodsmentioning

confidence: 99%

Separation of intramembrane charging components in low-calcium solutions in frog skeletal muscle.

Huang

1991

The Journal of General Physiology

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A B S T R A C T The inactivation of charge movement components by small (-100 to -70 mV) shifts in holding potential was examined in voltage-clamped intact amphibian muscle fibers in low [Ca2+], Mg2+-containing solutions. The pulse protocols used both large voltage excursions and smaller potential steps that elicited prolonged (q~) transients. Charge species were distinguished through the pharmacological effects of tetracaine. These procedures confirmed earlier observations in cut fibers and identified the following new properties of the q~ charge. First, %, previously defined as the tetracaine-sensitive charge, is also the component primarily responsible for the voltage-dependent inactivation induced by conditions of low extracellular [Ca2+]. Second, this inactivation separates a transient that includes a "hump" component and which has kinetics and a voltage dependence distinct from the monotonic decay that remains. Third, qv, previously associated with delayed charge movements, can also contribute significant charge transfer at early times. These findings suggest that the parallel inhibition of calcium signals and charge movements reported in low [Ca z+] solutions arises from influences on q~ charge (Brum et al., 1988a, b). They also reconcile reports that implicate tetracainesensitive (q~) charge in excitation-contraction coupling with evidence that early intramembrane events are also involved in this process . Finally, they are relevant to hypotheses of possible feedback or feed-forward roles of q~ in excitation--contraction coupling,

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“…In the preceding paper (Hodgkin & Nakajima, 1972) we showed that the low-frequency capacity of frog muscle fibres increases with diameter as expected if current spreads throughout most of the transverse tubular system (T-system). This article is concerned with the effect of diameter and detubulation on the capacity determined from the foot of the action potential.…”

Section: Introductionmentioning

confidence: 99%

Analysis of the membrane capacity in frog muscle

Hodgkin¹,

Nakajima²

1972

The Journal of Physiology

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121

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SUMMARY1. The membrane capacity (Cf) was determined from the conduction velocity and the time constant of the foot of the action potential in frog's skeletal muscle.2. In normal fibres Cf was 2 6 ,tF/cm2, and the value was almost constant over a range of diameter from 55 to 140 Au.3. In fibres, in which the transverse tubular system was disconnected from the surface by the glycerol treatment, CQ was 0'9 ,UF/cm2 and was fairly constant over a range of diameter from 60 to 130,u. The low frequency capacity in glycerol-treated fibres was 1-9 ,uF/cm2.4. These results as well as those obtained at low frequencies were consistent with the electrical model proposed by Adrian, Chandler & Hodgkin (1969).5. Analysis in terms of the model and of Peachey's (1965) data on tubular dimensions led to the following quantitative conclusions. The capacities of the surface membrane (Cs) and of the tubular wall (Cw) are both about 1 /zF/cm2. The conductances of the surface membrane (Gs) and tubular wall (Gw) are ca. 011 and 0 03 mmho/cm2, respectively. The conductivity of the luminal fluid in the tubules is ca. 6 mmho/cm.

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The effect of diameter on the electrical constants of frog skeletal muscle fibres

Cited by 193 publications

References 27 publications

Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

Separation of intramembrane charging components in low-calcium solutions in frog skeletal muscle.

Analysis of the membrane capacity in frog muscle

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