On the mechanism by which calcium and magnesium affect the spontaneous release of transmitter from mammalian motor nerve terminals

Hubbard, J. I.; Jones, S. F.; Landau, E. M.

doi:10.1113/jphysiol.1968.sp008413

Cited by 210 publications

(132 citation statements)

References 41 publications

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“…Dodge & Rahamimoff (1967) Hubbard et al (1968a) and Cooke et al (1973). Almost all the data presented in this paper can be fitted reasonably well to the sum of a linear function and a fourth power function of [Ca]o.…”

Section: Experiments With Cobalt Ringermentioning

confidence: 71%

“…frequency is determined at least in part by the resting calcium concentration inside the pre-synaptic terminal then the calcium dependence of evoked release when Ca entry is small (and excursions of the [Ca] [Ca], rather than the fourth power dependence that Miledi & Thies (1971) assume. Indeed the observation of Hubbard et al (1968a) and Cooke et al (1973) …”

Section: Experiments With Cobalt Ringermentioning

confidence: 99%

“…Previous studies on the relationship between evoked transmitter release and the external calcium concentration ([Ca]o) (Jenkinson, 1957;Dodge & Rahamimoff, 1967;Hubbard et al 1968a;Cooke et al 1973) (Curtis, 1963;Miledi & Thies, 1971), but also with calcium leakage from the preparation (Shanes & Bianchi, 1959;Miledi & Thies, 1971 from the Ringer lowered the [Ca]o to about 10-5 M. In all solutions the concentration of magnesium was raised to 2 mm to reduce the likelihood of action potential conduction failure (Dodge & Rahamimoff, 1967) and calcium chloride replaced isotonically by sodium chloride. Samples of the Ringer surrounding the preparation showed that nominally zero-calcium Ringer in fact contained about 10-5 M free calcium.…”

Section: Experiments In Unbuffered Ringermentioning

confidence: 99%

“…This together with poor sealing of the electrode tip into the muscle fibre in low calcium solutions (Hubbard et al 1968a) and the ensuing low m.e.p.p. amplitude probably means that measurements of m are underestimates.…”

Section: Experiments With Cobalt Ringermentioning

confidence: 99%

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The dependence of evoked transmitter release on external calcium ions at very low mean quantal contents

Crawford¹

1974

The Journal of Physiology

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SUMMARY1. The mean quantal content of the frog end-plate potential was examined under conditions that reduced evoked transmitter release to very low values.2. When the calcium concentration of the Ringer is reduced below 104 M a deviation occurs from the fourth power dependence of the mean quantal content (m) on the calcium concentration such that more quanta are released than is expected from the behaviour of m at higher calcium concentrations.3. At 1O-5 M this extra quantal release is more than two orders of magnitude greater than that predicted by the fourth power relationship.4. The calcium dependence of very low values of m was studied in low calcium Ringer in which the calcium was buffered by either citrate or EDTA. It was found that in the fourth power dependence of m on the external calcium concentration changes rather suddenly to an approximately linear dependence.5. The inclusion of small concentrations of cobalt in the Ringer was found to reduce m to very low values even in the presence of millimolar concentrations of calcium.6. The fourth power dependence of m on the external calcium concentration at high values of m was unaffected by the presence of cobalt. At low quantal contents the transition to a linear dependence on external calcium was again seen, but was shifted to calcium concentrations that did not require buffering.7. The fourth power to linear transition is discussed in terms of its relevance to the relationship between m and the m.e.p.p. frequency.

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Section: Experiments With Cobalt Ringermentioning

confidence: 71%

Section: Experiments With Cobalt Ringermentioning

confidence: 99%

Section: Experiments In Unbuffered Ringermentioning

confidence: 99%

Section: Experiments With Cobalt Ringermentioning

confidence: 99%

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The dependence of evoked transmitter release on external calcium ions at very low mean quantal contents

Crawford¹

1974

The Journal of Physiology

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“…Nelson & Sanchez, 1962;Landau & Nachshen, 1975). In contrast, the spontaneous release of transmitter at frog and rat neuromuscular junctions is increased by extracellular acidification (Hubbard, Jones & Landau, 1968;Landau & Nachshen, 1975;Cohen & van der Kloot, 1976). The nature of these opposite effects of extracellular pH on evoked and spontaneous ACh release is unknown.…”

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confidence: 83%

Regulation of acetylcholine release by intracellular acidification of developing motoneurons in Xenopus cell cultures

Chen

1998

The Journal of Physiology

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The effects of intracellular pH changes on the acetylcholine (ACh) release and cytoplasmic Ca2+ concentration at developing neuromuscular synapses were studied in Xenopus nerve‐muscle co‐cultures. Spontaneous and evoked ACh release of motoneurons was monitored by using whole‐cell voltage‐clamped myocytes. Intracellular alkalinization with 15 mm NH4Cl slightly reduced the frequency of spontaneous synaptic currents (SSCs). However, cytosolic acidification following withdrawal of extracellular NH4Cl caused a marked and transient increase in spontaneous ACh release. Another method of cytosolic acidification was used in which NaCl in Ringer solution was replaced with weak organic acids. The increase in spontaneous ACh release paralleled the level of intracellular acidification resulting from addition of these organic acids. Acetate and propionate but not isethionate, methylsulphate and glucuronate, caused an increase in intracellular pH and a marked increase in spontaneous ACh release. Impulse‐evoked ACh release was slightly augmented by intracellular alkalinization and inhibited by cytosolic acidification. Cytosolic acidification was accompanied by an elevation in the cytoplasmic Ca2+ concentration ([Ca2+]i), resulting from both external Ca2+ influx and intracellular Ca2+ mobilization. In contrast, the increase in [Ca2+]i induced by high K+ was inhibited by cytosolic acidification. We conclude that cytosolic acidification regulates spontaneous and evoked ACh release differentially in Xenopus motoneurons, increasing spontaneous ACh release but inhibiting evoked ACh release.

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Guanidine and Neuromuscular Transmission

Kamenskaya¹

1975

Arch Neurol

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The effect of guanidine on the neuromuscular transmission in human intercostal and mouse diaphragm muscle in vitro during repetitive nerve stimulation was studied. The drug greatly increased the release of acetylcholine (ACh) quanta by nerve impulses at low frequencies of nerve stimulation and at the beginning of tetani at high frequencies of stimulation. The effect was shown to be produced by an increase in fractional release from an unchanged store of ACh quanta available fro immediate release. This seems to explain why guanidine has a poor therapeutic effect in myasthenia gravis but a good effect in the myasthenic syndrome.

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On the mechanism by which calcium and magnesium affect the spontaneous release of transmitter from mammalian motor nerve terminals

Cited by 210 publications

References 41 publications

The dependence of evoked transmitter release on external calcium ions at very low mean quantal contents

The dependence of evoked transmitter release on external calcium ions at very low mean quantal contents

Regulation of acetylcholine release by intracellular acidification of developing motoneurons in Xenopus cell cultures

Guanidine and Neuromuscular Transmission

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