On the blockade of acetylcholine release at mouse motor nerve terminals by beta-bungarotoxin and crotoxin

E.G. Rowan, K.E. Pemberton, Alan L. Harvey

Research output: Contribution to journalArticle

Abstract

1. beta-Bungarotoxin and crotoxin are phospholipose A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preparations. 2. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. 3. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by beta-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K(+)-induced depolarization and by the Ca2(+)-ionophore A23187. 4. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.
LanguageEnglish
Pages301-304
Number of pages3
JournalBritish Journal of Pharmacology
Volume100
Issue number2
Publication statusPublished - Jun 1990

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Crotoxin
Bungarotoxins
Action Potentials
Acetylcholine
Ionophores
Calcimycin
Neurotoxins
varespladib methyl

Keywords

  • acetylcholine release
  • motor nerve terminals
  • beta-bungarotoxin
  • crotoxin

Cite this

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abstract = "1. beta-Bungarotoxin and crotoxin are phospholipose A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preparations. 2. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. 3. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by beta-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K(+)-induced depolarization and by the Ca2(+)-ionophore A23187. 4. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.",
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On the blockade of acetylcholine release at mouse motor nerve terminals by beta-bungarotoxin and crotoxin. / Rowan, E.G.; Pemberton, K.E.; Harvey, Alan L.

In: British Journal of Pharmacology, Vol. 100, No. 2, 06.1990, p. 301-304.

Research output: Contribution to journalArticle

TY - JOUR

T1 - On the blockade of acetylcholine release at mouse motor nerve terminals by beta-bungarotoxin and crotoxin

AU - Rowan, E.G.

AU - Pemberton, K.E.

AU - Harvey, Alan L.

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N2 - 1. beta-Bungarotoxin and crotoxin are phospholipose A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preparations. 2. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. 3. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by beta-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K(+)-induced depolarization and by the Ca2(+)-ionophore A23187. 4. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.

AB - 1. beta-Bungarotoxin and crotoxin are phospholipose A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preparations. 2. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. 3. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by beta-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K(+)-induced depolarization and by the Ca2(+)-ionophore A23187. 4. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.

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KW - crotoxin

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