Abstract

Ranvier nodes of single frog sciatic nerve fibers and desheathed bundles of frog tibialis nerve have been exposed to several compounds known to react with the acetylcholine system. The effects on electrical activity and on membrane properties have been studied. Eserine, a strong inhibitor of acetylcholinesterase, reversibly blocks conduction at Ranvier nodes in concentrations of 200–300 μg/ml within 30 sec; on intact frog sciatic nerve 20–30 min are required to obtain the same result with eserine at 3–5 mg/ml. 1.5 to 15 μg/ml eserine increases the spike amplitude and prolongs its descending phase. Lipid-soluble dimethyl aminoethyl acetate, when applied to Ranvier nodes at 1 mg/ml, increases spike height and prolongs the descending phase. When applied in combination with eserine (1.5 μg/ml) it blocks conduction reversibly. A lipid-soluble quaternary ammonium compound, pyridine-aldoxime dodeciodide blocks conduction of Ranvier nodes; at 10 −6 M the effect is reversible, while at 5·10 −6 it becomes irreversible. At lower concentrations (10 −7 M pyridine-aldoxime dodeciodide increases the amplitude and duration of the spike. Pyridine-aldoxime dodeciodide and other lipid-soluble quaternary ammonium compounds, applied to desheathed frog tibialis nerve at concentrations which do not affect the resting potential, increase the permeability to sodium, that to potassium appears slightly decreased. The mechanism of the action of these compounds is discussed. The effects offer new evidence for the role of acetylcholine in the conduction of nerve impulses.

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