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

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

Research output: Contribution to journalArticle

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 mu-conotoxin GIIIB (0.4-2.0 microM) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. 2. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and mu-conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. 3. The apparent block of K+ current by low concentrations of TTX and mu-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 pages3
JournalBritish Journal of Pharmacology
Volume106
Issue number1
Publication statusPublished - May 1992

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Conotoxins
Tetrodotoxin
Sodium
Neuromuscular Junction
Acetylcholine
conotoxin GIII

Keywords

  • tetrodotoxin
  • mu-conotoxin
  • k+ channels
  • na+ channels
  • neuromuscular junction
  • neurotransmission
  • acetylcholine release

Cite this

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title = "Apparent block of K+ currents in mouse motor nerve terminals by tetrodotoxin, mu-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 mu-conotoxin GIIIB (0.4-2.0 microM) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. 2. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and mu-conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. 3. The apparent block of K+ current by low concentrations of TTX and mu-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, mu-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, 05.1992, p. 91-94.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Apparent block of K+ currents in mouse motor nerve terminals by tetrodotoxin, mu-conotoxin and reduced external sodium

AU - Braga, M.F.M.

AU - Anderson, A.J.

AU - Harvey, A.L.

AU - Rowan, E.G.

PY - 1992/5

Y1 - 1992/5

N2 - 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 mu-conotoxin GIIIB (0.4-2.0 microM) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. 2. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and mu-conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. 3. The apparent block of K+ current by low concentrations of TTX and mu-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.

AB - 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 mu-conotoxin GIIIB (0.4-2.0 microM) selectively decreased the amplitude of the component of perineural waveforms associated with nerve terminal K+ currents, without affecting the main Na+ spike. 2. Intracellular recording of endplate potentials (e.p.ps) and miniature endplate potentials (m.e.p.ps) from triangularis sterni preparations revealed that TTX and mu-conotoxin GIIIB depressed the evoked quantal release of acetylcholine without significant effects on m.e.p.p. amplitude, frequency or time constant of decay. 3. The apparent block of K+ current by low concentrations of TTX and mu-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.

KW - tetrodotoxin

KW - mu-conotoxin

KW - k+ channels

KW - na+ channels

KW - neuromuscular junction

KW - neurotransmission

KW - acetylcholine release

UR - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1907466/pdf/brjpharm00218-0095.pdf

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