SOME twenty-five years ago Masland and Wigton1 showed that antidromic action potentials could be recorded from the ventral roots of cats during the muscular contraction provoked by the intra-arterial injection of acetylcholine. As a result of these experiments they suggested that acetylcholine might have an excitant effect on motor-nerve terminals. Later work2 has shown that many other quaternary ammonium compounds have the same ability to provoke antidromic action potentials in motor nerves. In particular Werner2 has shown, by ingenious but indirect means, that these drug effects are not due to excitation of the terminals by synchronous muscle action potentials. Despite these experiments which seem most satisfactorily explained by the presence of some cholinoceptive sites on the nerve terminals3, it has recently been claimed that at the present time there is no direct evidence for an action of acetylcholine on motor-nerve terminals4. This problem is of special interest, for an excitant action of the acetylcholine released by nerve impulses on nerve terminals is the central feature of a new hypothesis of transmitter release at ganglionic and neuromuscular junctions put forward by Koelle5. This excitant action is thought to release further acetylcholine in a sort of positive feed-back action.
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