Dual effects of ether on end‐plate currents.

Abstract

The effects of diethyl ether (ether) on miniature end-plate currents (m.e.p.c.s) and on acetylcholine-activated end-plate channels were measured in toad sartorius muscle fibers with voltage-clamp and extracellular recording techniques. At low concentrations (< 20 mM) ether made m.e.p.c.s decay faster than normal. At high concentrations (> 40 mM), the decay of m.e.p.c.s was slower than normal. With all concentrations, the decay remained exponential with single time constant, .tau.D. At low concentrations ether did not affect the growth phase of m.e.p.c.s and only slightly reduced the amplitude of m.e.p.c.s. At the higher concentrations, the growth phase was slowed and m.e.p.c.s were significantly reduced in amplitude. Ether at all concentrations (5-70 mM) reduced end-plate channel lifetime, the effect increasing with ether concentrations. Ether did not significantly alter the elementary channel conductance or the acetylcholine null (reversal) potential. Curare reduced .tau.D which had been prolonged by high concentrations of ether. Ether itself at high concentrations caused a reduction in .tau.D increased by neostigmine. It is proposed that high concentrations of ether inhibit acetylcholine hydrolysis by acetylcholinesterase. The effect of ether in reducing end-plate channel lifetime and reducing m.e.p.c. amplitude, without significantly altering the normal voltage and temperature sensitivity of channel lifetime, is consistent with the proposal that ether reduces the stability of open end-plate channels.