The nature and origin of calcium‐insensitive miniature end‐plate potentials at rodent neuromuscular junctions.

Lupa, M T; Tabti, Nacira; Thesleff, S.; Vyskočil, F.; Yu, Shan Ping

doi:10.1113/jphysiol.1986.sp016346

Cited by 47 publications

(16 citation statements)

References 31 publications

(34 reference statements)

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“…Acid Tyrode solution inhibited both the quantal size increase by hypertonic treatment and the higher frequency of giants produced by emetine (Alkadhi, 1989). Third, both the large miniatures and the giant MEPPs (Lupa, Tabti, Thesleff, Vyskocil & Yu, 1986) are reduced in size a few minutes after exposure to vesamicol.…”

Section: Large Quanta and Giant Miniaturesmentioning

confidence: 99%

“…Inhibition of high affinity choline transport Another approach was to use known inhibitors of the HAChT such as HC-3 (Elmqvist & Quastel, 1965;Yamamura & Snyder, 1973 (Elmqvist & Quastel, 1965;Lupa et al 1986). HC-3 also inhibits ACh transport into synaptic vesicles, but only at higher concentrations (IC50 = 300; Anderson et al 1983a, b).…”

Section: Effect Of Anticholinesterasementioning

confidence: 99%

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Increasing quantal size at the mouse neuromuscular junction and the role of choline.

Kloot

1991

The Journal of Physiology

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SUMMARY1. In frog a variety of treatments have been shown to increase quantal size at the neuromuscular junction (NMJ), apparently by releasing more acetylcholine (ACh) per quantum. The present experiments were undertaken to see whether similar changes occur at the mouse NMJ.2. None of the hormones tested, adrenaline, insulin or corticosteroids, significantly increased quantal size at the mouse NMJ.3. Soaking diaphragms in hypertonic solution (about 475 mosmol/kg) for 15-30 min roughly doubled the size of miniature endplate potentials (MEPPs), miniature endplate currents (MEPCs), and uniquantal endplate potentials (EPPs). We will refer to these as 'large quanta'. Note that all of the measurements were made after returning the preparation to normal (Tyrode) solution.4. In frog hypertonic solution made with sodium gluconate replacing NaCl increases quantal size four-rather than two-fold. In mouse there was little difference in the effects of solutions made with the two anions. In Cl--free hypertonic solution, made with sodium gluconate and SO42-solutions, quantal size increase is somewhat less, so there may be a role for Cl-in enlarging quantal size.5. After hypertonic treatment, quantal size remained elevated for at least 1 h and then gradually declined back to usual levels. The data suggest a gradual decrease in mean quantal size, rather than the appearance of a new subpopulation of smaller quanta.6. Hypertonic treatment did not change the endplate depolarization in response to ionophoretically applied ACh. This suggests that the increased quantal size is not due to a postsynaptic change. Large MEPP's disappear in the presence of tubocurarine and reappear when the drug is washed away.7. Vesamicol is an inhibitor of active ACh uptake into isolated synaptic vesicles.5 #m-vesamicol has no detectable postjunctional effect. However, when vesamicol was included in the Tyrode and the hypertonic solutions the increase in quantal size was blocked. This is further evidence that the large quanta are produced by the release of more ACh per quantum. 8. Even when added after the hypertonic treatment, vesamicol soon decreased quantal size back to the normal level. Two other inhibitors of active ACh uptake into vesicles, tetraphenylboron (TPB) and hexanitrodiphenylamine (HNPA) also de-MS 8417 S. P. YU AND W. VAN DER KLOOT creased quantal size after hypertonic treatment, apparently by a presynaptic action. This suggests that the additional ACh that produces large miniatures may be incorporated into the quanta shortly before release.9. Experiments were undertaken to test the hypothesis that the additional ACh added to the quanta is newly synthesized transmitter, produced by the acetylation of choline brought into the terminal by the high-affinity choline transport system (HAChT). The formation of large quanta was blocked when the solutions contained hemicholinium-3 (HC-3), an inhibitor of HAChT. At the concentrations used, HC-3 had no notable effect on the postjunctional acetylcholine receptor (AChR). After quantal size was incre...

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Section: Large Quanta and Giant Miniaturesmentioning

confidence: 99%

Section: Effect Of Anticholinesterasementioning

confidence: 99%

Increasing quantal size at the mouse neuromuscular junction and the role of choline.

Kloot

1991

The Journal of Physiology

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“…Unlike the frequency of MEPPs, the frequency of GMEPPs is neither affected by nerve terminal depolarization, nor by changes in extracellular calcium concentration [4,5]. Rather it seems to reflect changes in the presynaptic terminal namely an intracellular Ca 2+ dysregulation [1,6,7]. In 1996, Sellin and colleagues [8] suggested a possible origin of these giant events.…”

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confidence: 97%

The giant miniature endplate potentials frequency is increased in aged rats

Pousinha

Correia

Sebastião

et al. 2015

Neuroscience Letters

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“…The slow potentials are caused by intermittent spontaneous release of ACh from the motor nerve terminal. The released ACh comes from the same pool of ACh as that responsible for normal MEPPs and for impulse-evoked EPPs since blockade of ACh synthesis by hemicholinium reduces the three kinds of ACh potentials in parallel (Lupa, Tabti, Thesleff, Vyskocil & Yu, 1986). Furthermore, it is likely that the ACh causing the slow potentials has a synaptic vesicular origin since blockade of the transport of ACh from the cytoplasm into synaptic vesicles by the drug vesamicol (AH5 183) abolishes the appearance of slow potentials ).…”

Section: Effects On Transmitter Releasementioning

confidence: 99%

Botulinal Neurotoxins as Tools in Studies of Synaptic Mechanisms

Thesleff

1989

Exp Physiol

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The nature and origin of calcium‐insensitive miniature end‐plate potentials at rodent neuromuscular junctions.

Cited by 47 publications

References 31 publications

Increasing quantal size at the mouse neuromuscular junction and the role of choline.

Increasing quantal size at the mouse neuromuscular junction and the role of choline.

The giant miniature endplate potentials frequency is increased in aged rats

Botulinal Neurotoxins as Tools in Studies of Synaptic Mechanisms

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