Non-quantal acetylcholine release at mouse neuromuscular junction: Effects of elevated quantal release and aconitine

Abstract

The rate of non-quantal acetylcholine (ACh) release was estimated at the mouse neuromuscular junction by observing the effect of (+)-tubocurarine on endplate membrane potential or current in preparations pretreated with an irreversible anti-acetylcholinesterase (anti-AChE). Voltage clamping was an effective method for measuring nonquantal release. Non-quantal release was markedly inhibited by 10 μM aconitine. Non-quantal release was not significantly increased by 10 μM dihyroouabain (DHO). (It has been reported that ouabain increases the leak.) Non-quantal release was roughly doubled following exposure to hypertonic solution or to elevated K +-solution. This is in accord with the hypothesis that the leak is by way of ACh transporters incorporated into the terminal membrane following exocytosis, but other interpretations remain to be tested.