Effects of calcium on the conductance change of the end‐plate membrane during the action of transmitter

Takeuchi, Noriko

doi:10.1113/jphysiol.1963.sp007137

Cited by 176 publications

(73 citation statements)

References 36 publications

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“…Both of these kinases phosphorylate the ACh receptor (Huganir & Greengard, 1987;. Further, acetylcholine-gated endplate channels are permeable to calcium (Takeuchi, 1963). Therefore, calcium influx occurs at the endplate during exposure to nicotinic agonists, which in turn causes an elevation of the intracellular ionized calcium concentration near the inner surface of the postsynaptic membrane (Parsons & Nastuk, 1969;Manthey, 1974).…”

Section: Discussionmentioning

confidence: 99%

Staurosporine inhibits the extent of acetylcholine receptor recovery from carbachol‐induced desensitization in snake twitch fibres

Hardwick

Coniglio

Parsons³

1991

British J Pharmacology

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1 The effect of the protein kinase inhibitor, staurosporine, on the extent and time course of recovery following carbachol-induced desensitization was studied in snake twitch-muscle fibres maintained in an isotonic potassium propionate solution and voltage-clamped to + 30 mV. 3 Staurosporine also produced a concentration-dependent (10nM to 0.5 pM) decrease in the amplitude of a second carbachol-induced current, following a wash period, as compared to the amplitude of the current produced by the initial carbachol application. Pretreatment with 0.5,UM K252a, another wide spectrum protein kinase inhibitor, also decreased the extent of recovery of the response to a second carbachol application following desensitization.4 Staurosporine pretreatment (0.5jUM) had no effect on either the kinetics of receptor-channel gating or the initial endplate sensitivity to agonist. This was determined by comparing the amplitude of the carbachol (540Mm)-induced currents and the amplitude and decay rate of m.e.p.cs in control and staurosporine-treated fibres. 5 Staurosporine had no effect on the time course of desensitization onset produced during the initial application of 540piM carbachol or the depth of desensitization produced by the end of a 2-3 min exposure to 540pM carbachol.6 Elevation of the external calcium concentration from 1 to 10mM during the 540pM carbachol application completely antagonized the decreased extent of recovery of m.e.p.c. amplitude produced by pretreatment with 0.5JM staurosporine. 7 We suggest that phosphorylation of a population of acetylcholine receptors is required for complete recovery from desensitization, and that staurosporine inhibits the protein kinases responsible for this phosphorylation. 8 We further propose that a transient increase in intracellular calcium, produced by an increase in calcium influx through agonist-activated endplate channels, stimulates additional protein kinase activity, which in turn, antagonizes the effect of staurosporine-treatment on recovery.

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Section: Discussionmentioning

confidence: 99%

Staurosporine inhibits the extent of acetylcholine receptor recovery from carbachol‐induced desensitization in snake twitch fibres

Hardwick

Coniglio

Parsons³

1991

British J Pharmacology

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“…Other workers have shown that Ca2+ enters the endplate of vertebrate skeletal muscle as a consequence of agonist action on the endplate channels (Jenkinson & Nicholls, 1961;Takeuchi, 1963;Evans, 1974;Miledi et al, 1980). In our experiments with ECO the agonist is probably ACh released from the nerve terminals.…”

Section: Methodsmentioning

confidence: 59%

“…In unstimulated tissues, the amount released non-quantally from the nerve is about ten times greater than that released quantally (Miledi et al, 1983 & Vyskocil, 1979;Dolezal & Tucek, 1983;Stanley & Drachman, 1983) and is from the cytoplasm of the nerve (Molenaar et al, 1987 (Adams et al, 1986). In this regard, Jenkinson & Nicholls (1961) and Takeuchi (1963) reported abolition by Mg2+ of the local contracture normally found after ACh. Evans (1974) found that an increased [Mg2 ].…”

Section: Methodsmentioning

confidence: 84%

Accumulation of extracellular calcium at the endplate of mouse diaphragm after ecothiopate in vitro

Burd

Ferry

Smith

1989

British J Pharmacology

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Experiments were carried out to investigate the accumulation from the extracellular medium of 45Ca2+ by the endplate region of skeletal muscle. Mouse diaphragm muscle was incubated in physiological saline labelled with 45Ca at 37°C for periods of up to 1.5 h. The muscle was divided into junctional and non‐junctional portions and the Ca from the extracellular fluid accumulated at the endplate determined from the 45Ca content of the portions. The accumulation of extracellular Ca at the endplate region of muscles incubated in physiological saline alone was nil, but there was accumulation in the presence of the anticholinesterase ecothiopate iodide 0.5 × 10−6 m (ECO). Stimulation of the phrenic nerve at 0.02 Hz caused no further increase in accumulation, but reduced the amount of spontaneous fasciculation. In tetrodotoxin (TTX) 10−6 m, the accumulation was halved, and in 3.5 mM Mg2+ the accumulation was nil. Carbachol 10−4 m resulted in an accumulation of Ca similar to that in ECO. It is concluded that there was an accumulation of extracellular Ca following excitation of the nerve by stimulation at a low frequency and during the spontaneous fasciculations, and about half of the accumulation of extracellular Ca after ECO in the experiments was due to the postsynaptic action of ACh released non‐quantally from the nerve terminals.

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“…So, a local shortening of the MEP was attributed to a local increase of the Ca 2+ -concentration . Additionally, an influx of Ca 2+ by means of activated acetylcholine receptors (Takeuchi, 1963) or opened Na + -channels of subsynaptic folds (Beam et al, 1985) could be the cause of a local increase of the Ca 2+ -concentration.…”

Section: /4mentioning

confidence: 99%

About the morphological relationships of the sarcoplasmic reticulum in the sole plate area of the frog

Voigt¹,

Dauber²

2004

Tissue and Cell

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In the present investigation the sole plate area of motor end plates of the frog is ultrastructurally examined with different postfixation methods. We concentrated in this case on the proof of the smooth and rough sarcoplasmic reticulum of the sole plate. The relations of the smooth and rough sarcoplasmic reticulum to subsynaptic folds and the local T-system and its connections to diads and triads in the sole plate area are represented. The morphological differences between mammal and frog are pointed out. The possible functions of the sarcoplasmic reticulum in the myofibril-free sarcoplasm are discussed.

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Effects of calcium on the conductance change of the end‐plate membrane during the action of transmitter

Abstract: It is well known that the external concentration of calcium has a marked influence on the ordinary muscle membrane (

Cited by 176 publications

References 36 publications

Staurosporine inhibits the extent of acetylcholine receptor recovery from carbachol‐induced desensitization in snake twitch fibres

Staurosporine inhibits the extent of acetylcholine receptor recovery from carbachol‐induced desensitization in snake twitch fibres

Accumulation of extracellular calcium at the endplate of mouse diaphragm after ecothiopate in vitro

About the morphological relationships of the sarcoplasmic reticulum in the sole plate area of the frog

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