Significance of Membrane Calcium in Calcium-free and Potassium-rich Media

Koketsu, K.; Miyamoto, Shô

doi:10.1038/189403a0

Cited by 22 publications

(2 citation statements)

References 4 publications

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“…Post-tetanic potentiation of the end-plate potential is likely to be associated with a residual change in ionized calcium concentration at an important membrane site (Gage & Hubbard, 1966;Katz & Miledi, 1965). K+ may potentiate succinylcholine block by depletion of membrane Ca++ (Shanes & Bianchi, 1959;Koketsu & Miyamoto, 1961), rather than by virtue of the slight depolarization caused by this level of K+ (9.2 mM), or the moderate increase in m.e.p.p. frequency (Gage & Quastel, 1966).…”

Section: Discussionmentioning

confidence: 99%

Ionic Influences on Succinylcholine Blockade of the Mammalian Neuromuscular Junction

Freeman¹

1968

British Journal of Pharmacology and Chemotherapy

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Recent studies from a number of laboratories have been concerned with the delineation of factors affecting presynaptic events in neuromuscular transmission. In particular it seems that substances which block neuromuscular transmission by processes that include depolarization of the motor end-plate have important effects on the motor nerve terminals.These effects are not only produced by drugs such as succinylcholine and decamethonium, but are also shown by acetylcholine and its stable analogues.Hubbard, Schmidt & Yokota (1965) noted that acetylcholine reduced the quantal content of end-plate potentials (e.p.p.s.) without affecting miniature end-plate potential (m.e.p.p.) frequency. It appeared that acetylcholine did not depolarize the site of transmitter release, although the threshold of motor nerve terminals in paralysed preparations was reduced by acetylcholine. They concluded that acetylcholine depolarized the terminals at a site more proximal than that of transmitter release. Riker (1966) has produced evidence for a transitory depolarization of the motor nerve terminals by acetylcholine following close arterial injection in the cat. It is likely that Hubbard et al. (1965) did not observe this effect because of the slower rate of diffusion of acetylcholine into the isolated diaphragm preparation. Riker (1966) suggests that the motor nerve terminals undergo sequentially two stages of block in response to acetylcholinedepolarization and stabilization. This is a reformulation of the proposals of Jenden, Kamijo & Taylor (1954) and Thesleff (1955a) for a two-phase block of neuromuscular transmission by decomethonium and acetylcholine. The earlier proposals were, however, based on the assumption that these drugs had a postsynaptic site of action only.

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Section: Discussionmentioning

confidence: 99%

Ionic Influences on Succinylcholine Blockade of the Mammalian Neuromuscular Junction

Freeman¹

1968

British Journal of Pharmacology and Chemotherapy

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“…Much information supports the view that fundamentally excitation is produced by unbonding Ca from some structure by K: Effects on threshold, water entry into cells, Na or K entry into axons, salt retention by red cells, axon membrane resistance, width of axonal surface lamellae, Ca release from muscle or dorsal root ganglia, and axon structural changes due to polarization all depend on K : C a ratios in a relevant fashion (1,2,5,10,(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29). Hashimura and Wright have approached a similar formulation (30), and a recent paper by Spyropoulos approximately paraphrases this earlier stated hypothesis (31).…”

Section: Discussionmentioning

confidence: 99%

Phospholipid-Cholesterol Membrane Model

Tobias

Agin

Pawlowski

1962

The Journal of General Physiology

119

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A cephalin-cholesterol membrane model is described whose electrical resistance can be reversibly raised by CaCl2 or lowered by KCl or NaCl whether these ions are added to the membrane by mechanical immersion or are driven in electrically. Either KCl or NaCl acts antagonistically to CaCl2. Experiments with controlled pH indicate that the above effects depend somehow on combination of the cations with the phospholipid acidic groups. Also, they are correlated with decreased membrane hydration in CaCl2 solutions, and increased hydration in KCl or NaCl solutions. It is conjectured that cells may regulate their transsurface ion pathways and fluxes by K-Ca competition for negatively charged binding sites on plasma membrane phospholipid. It is regarded as a corollary to say that a fundamental event in excitation is displacement of membrane Ca from such a site by catelectrotonically propelled K.

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Membrane Responses of Frog Skeletal Muscle Fibers in Calcium‐Free Media

Koketsu

Noda

1962

J. Cell. Comp. Physiol.

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Significance of Membrane Calcium in Calcium-free and Potassium-rich Media

Cited by 22 publications

References 4 publications

Ionic Influences on Succinylcholine Blockade of the Mammalian Neuromuscular Junction

Ionic Influences on Succinylcholine Blockade of the Mammalian Neuromuscular Junction

Phospholipid-Cholesterol Membrane Model

Membrane Responses of Frog Skeletal Muscle Fibers in Calcium‐Free Media

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