Neuronal uptake processes for amine and amino acid transmitters

Abstract

The actions of released neurotransmitter substances on postsynaptic receptors are generally terminated by the rapid removal of the free transmitter from the synaptic cleft. The classic example of such a mechanism is the metabolic destruction of released acetylcholine by acetylcholinesterase at cholinergic junctions. However, it now seems likely that non-enzymic mechanisms operate at most other chemically transmitting synapses. Such mechanisms involve a physical removal of the released transmitter from its site of action, this removal being catalysed by a variety of different transport systems. The evidence for the existence and function of such uptake systems has been reviewed recently elsewhere (Iversen, 1967, 1971, 1972) and only the salient points will be described here. Most of the transport mechanisms that are associated with neurotransmitter function are located in the membranes of the presynaptic nerve terminals, so that removal of transmitter is equivalent to `recapture’, with the possibility that transmitter molecules may be released, recaptured, and re-used in many cases. There are, however, also examples of transmitter uptake occurring into sites other than the prejunctional terminal, see for example Gillespie, this symposium.