Literature DB >> 2600842

Giant miniature end-plate potentials at the untreated and emetine-treated frog neuromuscular junction.

K A Alkadhi1.   

Abstract

1. Intracellular recordings from the cutaneous pectoris muscle fibres of the frog showed that giant miniature end-plate potentials (gMEPPs) occurred in untreated preparations. Emetine (10 microM), after a 15-20 min delay, increased the frequency of gMEPPs. In both cases gMEPPs disappeared in the presence of (+)-tubocurarine. 2. There was no correlation between the frequency of gMEPPs and the frequency of normal MEPPs (nMEPPs) in untreated or emetine-treated fibres. 3. Tetraphenylborate (TPB, 50 microM) applied to muscles pre-treated with emetine caused the frequency and amplitude of both nMEPPs and gMEPPs to decrease gradually. All MEPPs disappeared in about 10 min. 4. Chloride permeability was modified by changing the pH of the Ringer solution. Changing the pH from 7.2 to 8.2 or 6.2, which in both cases caused marked increases in nMEPP frequency, had no significant effect on gMEPP frequency in untreated muscles. 5. Decreasing the pH from 7.2 to 6.2 blocked the ability of emetine to increase gMEPP frequency. Increasing the pH from 7.2 to 8.2 had no significant effect on emetine ability to increase gMEPP frequency. 6. Treatment with the Cl- channel blocker SITS (0.5 mM) had no effect on gMEPPs in untreated muscle or on the ability of emetine to increase the frequency of these potentials. 7. The Ca2+ sensitivity of gMEPPs in untreated or emetine-treated muscles was tested by treatments which are known to alter intracellular Ca2+. Raising extracellular Ca2+ (10 mM), treatment with Mn2+ (10 mM), Mg2+ (10 mM), K+ (7.5 mM), hypotonic solution, ouabain (0.2 mM) or ethanol (0.5 M), although causing profound changes in nMEPP frequency had no significant effect on gMEPP frequency in untreated fibres or on the ability of emetine to increase gMEPP frequency. 8. It is concluded that at the frog neuromuscular junction generation of the normally occurring or emetine-induced gMEPPs is independent of Ca2+ and does not seem to be influenced by changing membrane C1- permeability.

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Year:  1989        PMID: 2600842      PMCID: PMC1190587          DOI: 10.1113/jphysiol.1989.sp017627

Source DB:  PubMed          Journal:  J Physiol        ISSN: 0022-3751            Impact factor:   5.182


  37 in total

1.  Changes in spontaneous and evoked release of transmitter induced by the crotoxin complex and its component phospholipase A2 at the frog neuromuscular junction.

Authors:  B J Hawgood; S Santana de Sa
Journal:  Neuroscience       Date:  1979       Impact factor: 3.590

2.  A comparison of miniature end-plate potentials at normal, denervated, and long-term botulinum toxin type A poisoned frog neuromuscular junctions.

Authors:  M T Lupa; S P Yu
Journal:  Pflugers Arch       Date:  1986-11       Impact factor: 3.657

3.  Pharmacological characterization of the calcium-insensitive, intermittent acetylcholine release at the rat neuromuscular junction.

Authors:  N Tabti; M T Lupa; S P Yu; S Thesleff
Journal:  Acta Physiol Scand       Date:  1986-11

4.  Activity increases quantal size at the frog neuromuscular junction.

Authors:  W Van der Kloot; T E Van der Kloot
Journal:  Experientia       Date:  1985-01-15

5.  Miniature end-plate potentials in rat skeletal muscle poisoned with botulinum toxin.

Authors:  Y I Kim; T Lømo; M T Lupa; S Thesleff
Journal:  J Physiol       Date:  1984-11       Impact factor: 5.182

6.  Inhibition of non-quantal acetylcholine leakage by 2(4-phenylpiperidine)cyclohexanol in the mouse diaphragm.

Authors:  F Vyskocil
Journal:  Neurosci Lett       Date:  1985-09-06       Impact factor: 3.046

7.  4-aminoquinoline-induced 'giant' miniature endplate potentials at mammalian neuromuscular junctions.

Authors:  J Molgó; S Thesleff
Journal:  Proc R Soc Lond B Biol Sci       Date:  1982-01-22

8.  Is an acetylcholine transport system responsible for nonquantal release of acetylcholine at the rodent myoneural junction?

Authors:  C Edwards; V Dolezal; S Tucek; H Zemková; F Vyskocil
Journal:  Proc Natl Acad Sci U S A       Date:  1985-05       Impact factor: 11.205

9.  Botulinum toxin and 4-aminoquinoline induce a similar abnormal type of spontaneous quantal transmitter release at the rat neuromuscular junction.

Authors:  S Thesleff; J Molgó; H Lundh
Journal:  Brain Res       Date:  1983-03-28       Impact factor: 3.252

10.  Inhibition of [3H]acetylcholine active transport by tetraphenylborate and other anions.

Authors:  D C Anderson; S C King; S M Parsons
Journal:  Mol Pharmacol       Date:  1983-07       Impact factor: 4.436

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  5 in total

1.  Induction of giant miniature end-plate potentials during blockade of neuromuscular transmission by textilotoxin.

Authors:  H I Wilson; G M Nicholson; M I Tyler; M E Howden
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  1995-07       Impact factor: 3.000

2.  Impaired activity-dependent plasticity of quantal amplitude at the neuromuscular junction of Rab3A deletion and Rab3A earlybird mutant mice.

Authors:  Xueyong Wang; Qingbo Wang; Shuzhang Yang; Maja Bucan; Mark M Rich; Kathrin L Engisch
Journal:  J Neurosci       Date:  2011-03-09       Impact factor: 6.167

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

Authors:  S P Yu; W Van der Kloot
Journal:  J Physiol       Date:  1991-02       Impact factor: 5.182

4.  On the possible origin of giant or slow-rising miniature end-plate potentials at the neuromuscular junction.

Authors:  L C Sellin; J Molgó; K Törnquist; B Hansson; S Thesleff
Journal:  Pflugers Arch       Date:  1996-01       Impact factor: 3.657

5.  Regulation of quantal shape by Rab3A: evidence for a fusion pore-dependent mechanism.

Authors:  Xueyong Wang; Ramachandran Thiagarajan; Qingbo Wang; Teclemichael Tewolde; Mark M Rich; Kathrin L Engisch
Journal:  J Physiol       Date:  2008-06-26       Impact factor: 5.182

  5 in total

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