Insensitivity of activation delays in potassium and sodium channels to heavy water in Myxicola giant axons.

Schauf, C. L.

doi:10.1113/jphysiol.1983.sp014618

Cited by 11 publications

(15 citation statements)

References 28 publications

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“…In summary, the apparent discrepancy between Moore and Young (1981) and this report may simply be related to a difference in voltage clamp protocol, or the manner in which the results have been presented. Potassium activation kinetics similar to the results in this report have been observed in frog node of Ranvier (Palti et al, 1976;Begenisich, 1979), crayfish axons (Young and , and Myxicola axons (Schauf, 1983). It is tempting, therefore, to speculate that the lack of exact superposition is a feature common to the delayed rectifier channel in axons from all species.…”

Section: Discussionsupporting

confidence: 87%

Conditioning hyperpolarization delays in squid axon potassium channels

Clay¹

1986

Biophysical Journal

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Activation of potassium conductance in squid axons with membrane depolarization is delayed by conditioning hyperpolarization of the membrane potential. The delayed kinetics superpose with the control kinetics almost, but not quite, exactly following time translation, as demonstrated previously in perfused axons by Clay and Shlesinger (1982). Similar results were obtained in this study from nonperfused axons. The lack of complete superposition argues against the Hodgkin and Huxley (1952) model of potassium conductance. The addition of a single kinetic state to their model, accessible only by membrane hyperpolarization, is sufficient to describe this effect (Young and Moore, 1981).

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Section: Discussionsupporting

confidence: 87%

Conditioning hyperpolarization delays in squid axon potassium channels

Clay¹

1986

Biophysical Journal

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“…These effects were similar to those reported on Na¤ channels in crayfish giant axons (Schauf 1983;Alicata et al 1990), that is a reduction in current amplitude, a slowing of the time to peak current and a delay in inactivation. These effects have been explained in terms of an effect on the aqueous pore of the channel.…”

Section: Membrane Currents and [Ca¥]ésupporting

confidence: 87%

“…Studies in skeletal muscle concluded that a decrease in the amplitude of the contraction was the result of a decrease in the intracellular Ca¥ ([Ca¥]é) transient and a reduction in the myofilament sensitivity for Ca¥ (Allen et al 1984). DµO has also been reported to modulate electrical activity, decreasing and slowing axonal Na¤ and K¤ currents (Schauf, 1983;Alicata et al 1990). Prod'hom et al (1987) showed, that in the presence of Ca¥ channel agonists, D¤ caused greater block of long-lasting single calcium channel openings than H¤ in cardiac myocytes.…”

mentioning

confidence: 99%

Mechanisms Associated with the Negative Inotropic Effect of Deuterium Oxide in Single Rat Ventricular Myocytes

Hongo

Brette²,

Mohammad

et al. 2000

Experimental Physiology

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Deuterium oxide (D2O) is known to cause a negative inotropic effect in muscle although the mechanisms associated with this response in cardiac muscle are not well understood. We studied the effects of D2O in single rat ventricular myocytes in order to characterise the mechanisms associated with its negative inotropic effect and to assess its possible use as an acute modulator of microtubules. D2O rapidly reduced the magnitude of contraction in rat ventricular myocytes, and there was some recovery of contraction in the presence of D2O. Colchicine, an agent known to depolymerise microtubules, did not modify the effect of D2O. D2O decreased the L‐type Ca2+ current (ICa), measured under whole cell and perforated patch clamp conditions. Slowing of the time to peak and a delay in inactivation of ICa were observed. Intracellular calcium ([Ca2+]i) and sodium ([Na+]i) were measured using the fluorescent indicators fura‐2 and SBFI, respectively. The fall in contraction upon exposure to D2O was not associated with a fall in the [Ca2+]i transient; this response is indicative of a reduction in myofilament Ca2+ sensitivity. Both the [Ca2+]i transient and [Na+]i increased during the partial recovery of contraction in the presence of D2O. We conclude that a decrease in the myofilament sensitivity for Ca2+ and a reduction in Ca2+ influx via ICa are principally responsible for the negative inotropic effect of D2O in cardiac muscle. We found no evidence to explain the negative inotropic effect of D2O in terms of microtubule proliferation. In addition we suggest that acute application of D2O is not a useful procedure for the investigation of the role of microtubules in excitation‐contraction coupling in cardiac muscle.

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“…1, 2 and 4 show that the time to peak of the compound INa is increased by niflumic acid and TTX. Taking into account the differential effects of these drugs on (increase of h.), and they delay the INa turn-on (Armstrong & Bezanilla, 1974;Keynes & Rojas, 1976;Neumcke, Nonner & Stampfli, 1976;Chiu, 1977;Hahin & Goldman, 1978;Schauf, 1983;Taylor & Bezanilla, 1983). The delay in Na activation is usually interpreted as resulting from the existence of several closed states of the channels with an increased probability of channels being in the fully closed state at large hyperpolarizations.…”

Section: Turn-on Kineticsmentioning

confidence: 99%

Evidence for two transient sodium currents in the frog node of Ranvier.

Benoit¹,

Corbier²,

Dubois³

1985

The Journal of Physiology

105

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SUMMARY1. Na current (INa) was monitored in isolated voltage-clamped frog nodes of Ranvier in order to analyse the pharmacological and kinetic properties of fast and slow phases of inactivation.2. Niflumic acid (0-1-10 mM) and tetrodotoxin (0-3-30 nM) did not alter fast and slow inactivation time courses but preferentially reduced the amplitude of the fast phase of inactivation. The block of both phases of inactivation by niflumic acid and tetrodotoxin was well described if one assumed that more than one molecule of drug reacted with one channel.3. Fast and slow currents, corresponding respectively to fast and slow phases of inactivation, reversed at different potentials, had different threshold voltages of activation and the slopes of their steady-state inactivation curves were different. The recovery from inactivation of the compound INa could be described by the sum of two exponential (plus a delay) corresponding respectively to fast and slow currents.4. When calculated from INa recorded without and with niflumic acid or tetrodotoxin, the slow current activated about three times more slowly than the fast current.5. Large prehyperpolarizations delayed both the activation and the inactivation of the fast current but only the activation of the slow current.6. Lowering the temperature decreased the fast current but increased the slow current.7. We conclude that the inactivatable Na current of the nodal membrane is made up of two components (INa, and INa, ) corresponding to two different and interconvertible forms of the Na channel.

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Insensitivity of activation delays in potassium and sodium channels to heavy water in Myxicola giant axons.

Cited by 11 publications

References 28 publications

Conditioning hyperpolarization delays in squid axon potassium channels

Conditioning hyperpolarization delays in squid axon potassium channels

Mechanisms Associated with the Negative Inotropic Effect of Deuterium Oxide in Single Rat Ventricular Myocytes

Evidence for two transient sodium currents in the frog node of Ranvier.

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