Calcium inward current and related charge movements in the membrane of snail neurones.

Kostyuk, P. G.; Krishtal, O. A.; Pidoplichko, V I

doi:10.1113/jphysiol.1981.sp013557

Cited by 91 publications

(78 citation statements)

References 19 publications

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“…Activation of Ca2+ currents in other preparations such as snail neurones (Kostyuk et al 1981;Byerly & Hagiwara, 1982;Brown et al 1983;Byerly et al 1984a), pituitary cells (Hagiwara & Ohmori, 1982), rat sympathetic neurones (Belluzzi & Sacchi, 1989) and hippocampal neurones (Kay & Wong, 1987), has been shown to follow M2 kinetics. In contrast, chromaffin cell Ca2+ currents have been fitted with a two-exponential form (Fenwick et al 1982), cat sensory neurones Ca2+ currents were best fitted with a three-exponential form (Taylor, 1988 a) and a m5 form was required to fit Ca2+ currents in squid giant synapse (Llinas, Steinberg & Walton, 1981).…”

Section: Activation Of the Ca2+ Currentmentioning

confidence: 99%

“…Currents evoked from depolarized potentials should activate with roughly ml kinetics (Kostyuk et al 1981;Byerly et al 1984 a). This is so because a large fraction of Ca2+ channels is in a state that only needs to make one transition to reach the open state.…”

Section: Activation Of the Ca2+ Currentmentioning

confidence: 99%

“…It For tail current analysis neither linear leakage nor capacitive currents were subtracted from the recorded traces, and no filter was used. To evaluate the time course of ionic Ca2+ current activation, asymmetry currents presumably due to Ca2+ channel gating current (Adams & Gage, 1976;Kostyuk, Krishtal & Pidoplichko, 1981;Brown, Tsuda & Wilson, 1983) were eliminated by subtracting currents recorded in the presence of 200,cuM-Cd2+. After that, traces were digitally filtered with a cut-off frequency of 0-25 cycles per point.…”

Section: Introductionmentioning

confidence: 99%

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Activation kinetics of calcium currents in bull‐frog sympathetic neurones.

Sala

1991

The Journal of Physiology

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SUMMARY1. Calcium currents were recorded in dissociated bull-frog sympathetic neurones (BSNs) through patch pipettes using discontinuous voltage clamp. Activation kinetics were examined by analysing turn-on and turn-off currents.2. After short depolarizing pulses turn-off tail currents were fitted with the sum of two exponentials. The fast component (time constant, Tr t 240 jts at -40 mV) was undoubtedly due to the closure of calcium channels. The significance of a small and slower component is discussed.3. Neither activation nor deactivation time courses changed as channels inactivated during progressively longer pulses or when the holding potential was less negative. No specific component was selectively suppressed by these manipulations.4. Steady-state activation of the Ca2+ current was described by the Boltzmann distribution raised to the second power. Currents had an apparent threshold at -30 mV and were half-activated at + 5 mV.5. Calcium current turned on following m2 kinetics throughout the range of activation. The slowest time constant was around 1-2 ms between 0 and + 10 mV. Turn-on was faster at negative or more positive potentials.6. The time course of decay of tail currents became progressively faster at more negative potentials.7. The instantaneous current-voltages (I-V) curve was obtained from tail current measurements and fitted by a modified constant-field equation.8. The measured peak I-V curve could be reconstructed from the activation curve and the instantaneous I-V curve.9. The activation kinetics of the calcium current in BSNs were consistent with the existence of a single kinetic class of channels and can be described with a simple m2 Hodgkin-Huxley model.

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Section: Activation Of the Ca2+ Currentmentioning

confidence: 99%

Section: Activation Of the Ca2+ Currentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Activation kinetics of calcium currents in bull‐frog sympathetic neurones.

Sala

1991

The Journal of Physiology

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“…They do not contribute to the monotonically decaying Ca 2+ channel gating currents in neurons (Kostyuk et al, 1981), arthropod skeletal muscle (Gilly and Scheuer, 1984), and mammalian cardiac muscle (Bean and Rios, 1989), even though all these systems are activated by elevations of cytosolic Ca 2+. However, the latter systems are differently triggered indirectly by extracellular Ca 2 entry (Beuckelman and Wier, 1988;Fabiato, 1985;LopezLopez et al, 1995;Cannell et al, 1995;Sun et al, 1995).…”

Section: Introductionmentioning

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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“…It has been reported that Ca channels are 'washed out' during intracellular perfusion (Kostyuk, Krishtal & Pidoplichko, 1981;Byerly & Hagiwara, 1982) and 'run down' irreversibly after formation of an isolated membrane patch (Fenwick, Marty & Neher, 1982;Cavalie, Ochi, Pelzer & Trautwein, 1983).…”

Section: Introductionmentioning

confidence: 99%

Kinetic properties and selectivity of calcium‐permeable single channels in Aplysia neurones.

Chesnoy-Marchais¹

1985

The Journal of Physiology

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SUMMARY1. Two kinds of single channels, carrying inward currents even above the Na and Cl ion equilibrium potentials, were observed in outside-out patches from Aplysia neurones bathed in K-free internal and external solutions. The channel carrying the larger elementary current has been studied in detail.2. When the internal solution contained mainly CsCl, this channel usually inactivated during the first minutes following isolation of the membrane patch. However, when the internal solution contained NaCl instead of CsCl, the channel remained functional during several hours, thus allowing the present study.3. Na-Tris, NaCl-mannitol and Ca-Ba external substitution experiments showed that the channel studied is much more permeable to divalent cations than to sodium ions. 12. The possible relationships between this channel and previously described 'Ca channels' and 'slow inward currents' are discussed.

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Calcium inward current and related charge movements in the membrane of snail neurones.

Cited by 91 publications

References 19 publications

Activation kinetics of calcium currents in bull‐frog sympathetic neurones.

Activation kinetics of calcium currents in bull‐frog sympathetic neurones.

Kinetic isoforms of intramembrane charge in intact amphibian striated muscle.

Kinetic properties and selectivity of calcium‐permeable single channels in Aplysia neurones.

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