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 journalArticlepeer-review

16 Citations (Scopus)


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 ( and miniature endplate potentials ( 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.

Original languageEnglish
Pages (from-to)91-94
Number of pages4
JournalBritish Journal of Pharmacology
Issue number1
Publication statusPublished - 1 Jan 1992


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

Cite this