The influence of chloride on the ouabain-sensitive membrane potential and conductance of crayfish giant axons

Lieberman, Edward M.; Nosek, Thomas M.; Young, E.

doi:10.1007/bf00585878

Cited by 23 publications

(17 citation statements)

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“…In addition, there is a relatively complete set of data on the effects of external [K+l0 on "a' ], and [K'li (Strickholm and Wallin, 1967;Wallin, 1967a,b), specific ion transmembrane conductances (Strickholm and Clark, 1977;Lieberman, 1979), and the Na+/K'-coupled transport ratio (Lieberman and Nosek, 1976;Lieberman, 1979) in the crayfish giant axon. These data allow the estimation of Na+ and K' fluxes in a cell shown to be in steady state with respect to intracellular Na+, K' , and -P under various [K+l0 conditions.…”

Section: Discussionmentioning

confidence: 99%

“…In general terms, a system in steady state is one in which its composition is time invariant. The practical definition of the system steady state used in this study was the time invariance of the membrane potential, [Na+Ii, [KfIi (Wallin, 1967b;Lieberman and Nosek, 1976), and, as shown in this investigation, high-energy phosphate (-P) concentration for at least 3 h under control conditions. Under steady-state conditions, it is predicted that ionic fluxes and energy consumption by the transport system should be inversely related to the [K'],, a finding suggesting that both the Na+/K+ transport ratio and turnover rate are modulated to account for changes in transport electrogenicity.…”

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confidence: 99%

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Effect of Extracellular Potassium on Ouabain‐Sensitive Consumption of High‐Energy Phosphate by Crayfish Giant Axons: A Study of the Energy Requirement for Transport in the Steady State

Lieberman

Pascarella

Brunder

et al. 1990

Journal of Neurochemistry

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Crayfish axons exposed to a high or low extracellular K+ concentration ([K+]o) maintain intracellular Na+ and K+ concentrations constant, for up to 3 h, by adjusting both the Na+/K+ transport "coupling ratio" and turnover rate in compensation for changes in ion fluxes due to altered electrochemical gradients. These findings give rise to the prediction that the steady-state consumption of high-energy phosphate (approximately P) [ATP and phospho-L-arginine (Arg-P)] is inversely proportional to the [K+]o, i.e., directly proportional to the product of membrane conductance and magnitude of the transmembrane electrochemical gradients for Na+ and K+. This investigation was designed to test this hypothesis. The [K+]o did not influence total approximately P consumption (Q approximately P) of the axon. For a [K+]o between 0.5 and 21.6 mM, Q approximately P averaged 52.8 +/- 4.7%/h (n = 44) of the initial [ATP] + [Arg-P]. Unlike total Q approximately P, the ouabain-sensitive portion of Q approximately P was markedly influenced by [K+]o. In 0.5 mM K+o, ouabain poisoning reduced Q approximately P to 8%/h, a result indicating that 85% of the total Q approximately P was ouabain sensitive. For 1.35 mM K+o, the ouabain-sensitive portion was 66%; at 5.4 mM K+o, 45%; and at 13.5 mM K+o, 41%. There was a small but significant increase in the ouabain-sensitive Q approximately P at 21.6 mM K+o, compared with Q approximately P at 5.4 mM K+o. The pattern of effect of [K+]o on Q approximately P was similar to its effect on the electrical power content of the Na+ and K+ electrochemical gradients. In contrast to the generally accepted Na+ flux (JNa)/approximately P stoichiometry of 3, an actual ratio of JNa/approximately P stoichiometry of approximately 33:1 was calculated for the experiments reported here, a result suggesting that cells in a zero-membrane current steady state utilize efficient energy conservation mechanisms that may not operate under non-steady-state conditions.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Effect of Extracellular Potassium on Ouabain‐Sensitive Consumption of High‐Energy Phosphate by Crayfish Giant Axons: A Study of the Energy Requirement for Transport in the Steady State

Lieberman

Pascarella

Brunder

et al. 1990

Journal of Neurochemistry

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“…Inhibition of the pump with cardiac glycosides has been shown to increase membrane conductance (Geduldig, 1968). This alteration in membrane conductivity probably results from a secondary rearrangement of chloride ion concentrations following changes in the pump activity, which have been demonstrated in vitro in the membrane of crayfish giant axons (Lieberman et al, 1976).…”

Section: Neuronal Excitabilitymentioning

confidence: 92%

Changes in cation transport during affective illness: Do they have therapeutic implications?

Wood

1987

Human Psychopharmacology

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Changes in some of the specific mechanisms which transport cations across cell membranes have been demonstrated in patients suffering from affective illness. A number of novel strategies have been evaluated in the management of both mania and depression, based on the following observations: (1) State-related changes in cation transport; (2) The effects of established psychotherapeutic drugs upon cation transport; and (3) theories regarding control of membrane ion flux. This article reviews the background to these novel strategies and evaluates the possible significance of changes in a number of different cation transport systems to the treatment of the affective disorders.KEY worms-Cation transport, affective illness, vanadium, Na+, K+-ATPase neurotransmitters CATION TRANSPORT There is a difference between the prevailing concentrations of sodium and potassium on the two sides of cell membranes. The concentration of potassium inside the cell is high relative to the extracellular fluid, the gradient of sodium concentration being in the opposite direction (extracellular > intracellular). The concentration gradients are important to many aspects of cellular function and, in particular, are the basis of the potential difference that exists across the cell membrane. Each cation tends to 'leak' across the membrane down its own concentration gradient and active processes are necessary to pump ions back against the gradient in order that these concentration differences be maintained. The mechanisms of cation transportThere are three different groups of transport systems which facilitate the movement of cations across cell membranes (see Figure 1).(1) One group of systems are energy-dependent ion 'pumps'. These are complex enzymes, often made up of several subunits, which move one or more ions across the membrane, up a concentration gradient. The energy for this process comes from the linked hydrolysis of the high-energy bond of adenosine triphosphate (ATP)-the major store for cellular energy. These enzymes are known collectively as the ATPases. The best-characterized of these systems is the sodium-and potassiumdependent adenosinetriphosphatase (Na+, K+-ATPase), also known as the sodium pump.Another group of transport mechanisms link one energy-producing cation movement to a second energy-requiring cation shift. The best example of such a system is the Na+/K+ co-transport system which links the inward (extracellular fluid to cytoplasm) flux of sodium ions, down the sodium concentration gradient , to the energy-requiring process of inward movement of potassium ions up the potassium concentration gradient. The energy for this process comes initially from the maintenance of the sodium gradient by the sodium pump. There are also a number of channels spanning the membrane which facilitate the transport of particular ions. They can be controlled (opened or closed) either by changes in the potential difference across the membrane, by changes in the concentration of other ions, and by a number of drugs, hormones and other messenge...

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“…Part of the effects of VPA appear to be secondary to the depolarization produced by this anticonvulsant agent. The depolarization in response to VPA could be due to the decrease in membrane conductance (either to chloride or potassium) or to inhibition of the electrogenic Na+-Kt pump that makes a large contribution to the resting membrane potential of the crayfish giant axon (Lieberman and Nosek, 1976). In the present series of experiments, an impermeant anion (isethionate) was substituted for the chloride in the bathing medium in order to determine the role of chloride in the membrane response to VPA and DPH.…”

Section: Department Of Physiology Medical College Of Georgia Augustmentioning

confidence: 99%

“…The effect of VPA and DPH on electrogenic Na+-K+ active transport was assessed by using the Na+-K+ ATPase inhibitor ouabain to block active transport after application of either VPA or DPH. Lieberman and Nosek (1976) used the conductance equation, as described by Hodgkin and Huxley (1952) and modified by Kornacker (1969), to calculate the total pump current and Na+-K+ coupling ratio, as well as the resting sodium and potassium conductances, from the electrophysiologic characteristics of the axons. This analysis was utilized here to evaluate the effects of VPA and DPH on these membrane properties.…”

Section: Department Of Physiology Medical College Of Georgia Augustmentioning

confidence: 99%

How Valproate and Phenytoin Affect the Ionic Conductances and Active Transport Characteristics of the Crayfish Giant Axon

Nosek

1981

Epilepsia

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Summary: The purpose of this study was to determine the effect of valproic acid (VPA) and phenytoin (DPH) on chloride conductance and electrogenic Na+‐K+ active transport in the crayfish giant axon. Exposure of the axon to a medium containing no chloride (isethionate substitution) produced no change in the resting potential but significantly decreased the resting conductance and +dV/dtmax and increased the action potential duration. The response of axons bathed in a Cl‐‐free medium to VPA was not significantly different from that of axons bathed in Ch‐containing medium; the resting potential, total membrane conductance (gM), +dV/dtmax, and ‐dV/dtmax decreased, while the action potential duration increased. These results indicate that VPA does not produce its effects on membrane properties through an influence on chloride conductance. Similarly, DPH does not produce its effects through a change in chloride conductance; DPH decreases +dV/dtmax, ‐dV/dtmax, and gM, increases the duration of the action potential, and is without effect on the resting and action potentials with or without chloride in the bathing medium. Ouabain depolarized control axons and axons pretreated with VPA or DPH to an equal extent. From these data and other electrophysiologic characteristics of the axons, the resting Na+ and K+ conductances and the net pump current and coupling ratio were calculated. VPA significantly decreased gK but was without effect on gNa. That VPA was without effect on any property of the electrogenic Na+‐K+ active transport process indicates that the depolarization and decrease in total membrane conductance in response to VPA are due to the decrease in gK> produced by this compound. Even though VPA did not affect active transport at rest, it did suppress the response of active transport to drive, suggesting that VPA inhibits posttetanic potentiation. In contrast, DPH decreased g K and gNa so as to maintain the gnJgK ratio constant. This effect, coupled with a lack of an influence on the electrogenic active transport process, explains the absence of an effect of DPH on the resting membrane potential. The decrease in g M by DPH accounts for the increase in magnitude of the response to drive noted in the presence of DPH. These membrane effects suggest cellular mechanisms by which VPA and DPH can interfere with the spread of high‐frequency electrical activity away from an epileptic focus. RÉSUMÉ Le but de cette étude était de detérminer les effets de l'acide Valproïque (VPA) et de la Phénytoïne (DPH) sur la conductance du chlore et les transports actifs électrogéniques Na+/K+ de I'axone géant de l'écrevisse. L'immersion de I'axone dans un milieu dépourvu d'ions chlore (par substitution au moyen d'isothionate) ne modifie pas le potentiel de repos, mais diminue de facon significative la conductance de repos 1dV/dtmax et, augmente la durée du potentiel d'action. La réponse des axones plonges dans un milieu dépourvu d'ions CI en présence de VPA n'est pas significativement differente de celle obtenue en presence d'ions CI; le ...

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The influence of chloride on the ouabain-sensitive membrane potential and conductance of crayfish giant axons

Cited by 23 publications

References 23 publications

Effect of Extracellular Potassium on Ouabain‐Sensitive Consumption of High‐Energy Phosphate by Crayfish Giant Axons: A Study of the Energy Requirement for Transport in the Steady State

Effect of Extracellular Potassium on Ouabain‐Sensitive Consumption of High‐Energy Phosphate by Crayfish Giant Axons: A Study of the Energy Requirement for Transport in the Steady State

Changes in cation transport during affective illness: Do they have therapeutic implications?

How Valproate and Phenytoin Affect the Ionic Conductances and Active Transport Characteristics of the Crayfish Giant Axon

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