Oscillations of membrane potential in L cells

Okada, Yasunobu; Doida, Yukio; Roy, G.; Tsuchiya, Wakoh; Inouye, Ken; Inouye, Akira

doi:10.1007/bf01869957

Cited by 71 publications

(10 citation statements)

References 15 publications

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“…Similar hyperpolarizing responses have been found in non-excitable tissues, such as in cultured fibroblasts (Okada et al, 1977) and fertilized hamster eggs (26).…”

Section: Ca-dependent K Channels In Excitable and Non-excitable Tissuessupporting

confidence: 78%

II-6 Excitable Membrane-Animals

Takahashi¹

1984

Cell Struct. Funct.

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“…Similar hyperpolarizing responses have been found in non-excitable tissues, such as in cultured fibroblasts (Okada et al, 1977) and fertilized hamster eggs (26).…”

Section: Ca-dependent K Channels In Excitable and Non-excitable Tissuessupporting

confidence: 78%

II-6 Excitable Membrane-Animals

Takahashi¹

1984

Cell Struct. Funct.

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“…In the hamster egg it is thought that the primary mechanism for polyspermy block resides in the zona pellucida, which becomes impenetrable to sperm on account of the material(s) released from cortical granules; that is, zona reaction (21,22). Periodic hyperpolarizing responses have been found in fibroblastic L cells (23,24), macrophages (25,26), and sympathetic ganglion cells (27). They are suggested to be related to cell motility, such as phagocytosis of fibroblastic L cells (28) or the activation of chemotactic migration of macrophages (29).…”

Section: Discussionmentioning

confidence: 99%

Ca-mediated activation of a K current at fertilization of golden hamster eggs.

Miyazaki¹,

Igusa²

1982

Proc. Natl. Acad. Sci. U.S.A.

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“…The transmembrane electrochemical gradients established by these two cations have been implicated in several physiological responses, including the regulation of cell volume (1,2), nutrient cotransport (3)(4)(5)(6), and membrane excitability (7)(8)(9)(10). Because the steady-state K+ concentration reflects the sum of influx and efflux components, both active and passive, an alteration in the activity of one component must be accompanied by a compensating alteration in another if the cationic steady state is to be maintained (11).…”

mentioning

confidence: 99%

Reduction of K+ efflux in cultured mouse fibroblasts, by mutation or by diuretics, permits growth in K+-deficient medium.

Jayme¹,

Adelberg²,

Slayman³

1981

Proc. Natl. Acad. Sci. U.S.A.

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The mouse fibroblastic cell line LM(TK-) is unable to grow at external K+ concentrations below a threshold value of 0.4 mM. At subthreshold K+ concentrations, LM(TK-) cells rapidly lose intracellular K+ and eventually lyse. We have analyzed the pathwayprimarily responsible for K+ efflux under these experimental conditions and report its specific inhibition by two diuretics, furosemide and bumetanide. Bumetanide, an analog of furosemide, was a more potent inhibitor (by several orders of magnitude) than was furosemide itself. The effects of ouabain and bumetanide were additive, suggesting independence of diureticsensitive K+ efflux from Na+/K+ pump-mediated fluxes. Characterization of K+ efflux in LTK-5, a mutant derived from LM(TK-) and selected for its ability to grow at 0.2 mM K+, indicated that the mutant had lost the diuretic-sensitive K+ efflux pathway. Net Mammalian cells maintain a high steady-state K+ concentration and a low steady-state Na+ concentration relative to their surrounding physiological fluids. The transmembrane electrochemical gradients established by these two cations have been implicated in several physiological responses, including the regulation of cell volume (1, 2), nutrient cotransport (3-6), and membrane excitability (7-10). Because the steady-state K+ concentration reflects the sum of influx and efflux components, both active and passive, an alteration in the activity of one component must be accompanied by a compensating alteration in another if the cationic steady state is to be maintained (11). Should a particular flux become altered so that antagonistic fluxes are unable to compensate, the resulting change in intracellular cation concentration may be lethal to the cell. Such considerations were the basis for the selection of two K+ transport mutants that gained the ability to grow at a K+ concentration below that minimally required for parental cell growth (12). Both mutants proved capable of maintaining high intracellular K+ concentrations at reduced external K+ through changes in ouabain-insensitive K+ transport.One of the mutants, LTK-5, exhibited altered activity of a Na+-K+ cotransport system (12, 13) similar to that described in human (14, 15) and avian (16) erythrocytes and in Ehrlich cells (17-21) and murine fibroblasts (22,23). Specifically, in characterizing the mutant relative to its parent strain under conditions of K+ depletion and high external K+, Gargus and Slayman (13) noted that LTK-5 demonstrated enhanced furosemidesensitive, Na+-dependent K+ influx. For two reasons, however, it seemed unlikely that the increase in K+ influx was causally related to the ability of the mutant to survive selection. (i) When furosemide-sensitive K+ influx was measured as a function of the extracellular K+ concentration in both parent and mutant cells, it reached a half-maximal rate at 6 mM K+, considerably higher than the Km for the ouabain-sensitive Na+/K+ pump (1.3 mM). At 0.2 mM K+, the concentration used in the selection, furosemide-sensitive influx was barely detecta...

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Oscillations of membrane potential in L cells

Cited by 71 publications

References 15 publications

II-6 Excitable Membrane-Animals

II-6 Excitable Membrane-Animals

Ca-mediated activation of a K current at fertilization of golden hamster eggs.

Reduction of K+ efflux in cultured mouse fibroblasts, by mutation or by diuretics, permits growth in K+-deficient medium.

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