Blockade by 2,2',2''-tripyridine of the nicotinic acetylcholine receptor channels in embryonic Xenopus muscle cells

Br J Pharmacol. 1993 Sep;110(1):163-8. doi: 10.1111/j.1476-5381.1993.tb13787.x.

Abstract

1. The effects of 2,2',2''-tripyridine on the nicotinic acetylcholine (ACh) receptor channels were studied in the cultured myocytes of 1-day-old Xenopus embryos. 2. 2,2',2''-Tripyridine depressed the amplitude of iontophoretic ACh-induced current at a low frequency of 0.7 Hz stimulation and it not only decreased the initial responses but also enhanced the run-down of ACh-induced current at higher frequency stimulation of 7 Hz and 30 Hz. 3. Single ACh channel recordings showed that 2,2',2''-tripyridine decreased the channel conductance, the opening frequency and mean open time of both types of low- and high-conductance channels. 4. These results suggest that the blocking actions of 2,2',2''-tripyridine on ACh receptor channels in the skeletal muscle may contribute to the depression of the nerve-evoked contraction of the mouse diaphragm as reported previously.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / metabolism
  • Animals
  • Electric Stimulation
  • Electrophysiology
  • Ion Channels / drug effects
  • Iontophoresis
  • Membrane Potentials / drug effects
  • Muscles / drug effects
  • Muscles / embryology
  • Muscles / metabolism*
  • Neuromuscular Blocking Agents / pharmacology*
  • Nicotinic Antagonists*
  • Pyridines / pharmacology*
  • Xenopus

Substances

  • Ion Channels
  • Neuromuscular Blocking Agents
  • Nicotinic Antagonists
  • Pyridines
  • 2,2',2''-terpyridine
  • Acetylcholine