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.
|Number of pages||3|
|Journal||British Journal of Pharmacology|
|Publication status||Published - May 1992|
- k+ channels
- na+ channels
- neuromuscular junction
- acetylcholine release