Nerve terminal ATPase as possible trigger for neurotransmitter release

Abstract

WHEN a wave of depolarisation spreads down an axon and invades the nerve terminals a number of events rapidly occur and it is difficult to establish the one ultimately res ponsible for the release of neurotransmitter. There is strong evidence to support the contention that calcium ion influx is involved both in the release of acetylcholine¹ and of noradrenaline² but ion-exchange processes at the level of the vesicle not necessarily directly involving calcium have been proposed³ and the concept of regulation of release through changes in the activity of an adenosine triphos-phatase (ATPase) has also been invoked^4,5. This paper is concerned with the last possibility. Following the inward movement of sodium ions the inward movement of calcium ions to the enzyme on the inner edge of the nerve terminal membrane would be expected to inhibit the activity of sodium potassium-activated magnesium-dependent ATPase (Na,K-ATPase)⁶. Sodium depletion or the addition of ouabain to preparations in vitro would also be expected to inhibit Na K-ATPase activity. These three conditions of enzyme inhibition have all been shown to result in increased acetylcholine release^4,5.