Apparent block of K+ currents in mouse motor nerve terminals by tetrodotoxin, μ‐conotoxin and reduced external sodium

M. F. M. Braga, A.J. Anderson, A. L. Harvey, E. G. Rowan

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

In mouse triangularis sterni nerve‐muscle preparations, reduced extracellular Na+ concentrations and low concentrations of the Na+ channel blocking toxins tetrodotoxin (TTX, 18–36 nm) and μ‐conotoxin GIIIB (0.4–2.0 μm) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and μ‐conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. The apparent block of K+ current by low concentrations of TTX and μ‐conotoxin is probably not a direct effect on K+ channels but results from a decrease in the passive depolarization of nerve terminals following blockade of a small proportion of axonal Na+ channels.

LanguageEnglish
Pages91-94
Number of pages4
JournalBritish Journal of Pharmacology
Volume106
Issue number1
DOIs
Publication statusPublished - 1 Jan 1992

Fingerprint

Conotoxins
Tetrodotoxin
Sodium
Neuromuscular Junction
Acetylcholine
conotoxin GIII

Keywords

  • acetylcholine release
  • K channels
  • Na channels
  • neuromuscular junction
  • neurotransmission
  • tetrodotoxin
  • μ‐conotoxin
  • mu conotoxin
  • sodium ion
  • animal tissue
  • intracellular recording
  • nerve ending

Cite this

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title = "Apparent block of K+ currents in mouse motor nerve terminals by tetrodotoxin, μ‐conotoxin and reduced external sodium",
abstract = "In mouse triangularis sterni nerve‐muscle preparations, reduced extracellular Na+ concentrations and low concentrations of the Na+ channel blocking toxins tetrodotoxin (TTX, 18–36 nm) and μ‐conotoxin GIIIB (0.4–2.0 μm) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and μ‐conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. The apparent block of K+ current by low concentrations of TTX and μ‐conotoxin is probably not a direct effect on K+ channels but results from a decrease in the passive depolarization of nerve terminals following blockade of a small proportion of axonal Na+ channels.",
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Apparent block of K+ currents in mouse motor nerve terminals by tetrodotoxin, μ‐conotoxin and reduced external sodium. / Braga, M. F. M.; Anderson, A.J.; Harvey, A. L.; Rowan, E. G.

In: British Journal of Pharmacology, Vol. 106, No. 1, 01.01.1992, p. 91-94.

Research output: Contribution to journalArticle

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