Is an acetylcholine transport system responsible for nonquantal release of acetylcholine at the rodent myoneural junction?

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Abstract
Experiments were performed to investigate the effects on the spontaneous, nonquantal release of acetylcholine (ArCho) from motor nerve terminals of substances known to inhibit the AcCho transport system present in cholinergic synaptic vesicles. In mouse diaphragms, the hyperpolarization normally produced by d-tubocurarine in the endplate area of muscle fibers that had been treated by an anticholinesterase was partly or completely blocked by 2-(4-phenylpiperidino)cyclohexanol(AH5183, 0.1-1 .mu.M), quinacrine (0.1 .mu.M) and tetraphenylborate (1 .mu.M). Since the sensitivity of the subsynaptic area to ArCho was not changed, the block ofthe hyperpolarizing action of d-tubocurarine indicated an inhibition of the spontaneous, nonquantal release of AcCho. This was confirmed in experiments on rat diaphragm using direct radioenzymatic measurement on the ArCho released into theincubation medium. The release of AcCho from the innervated diaphragm was decreased by about 50% in the presence of AH5183 (0.01-1 .mu.M) and by 42% in the presence of quinacrine (0.1-1 .mu.M). The AcCho released was presumably neural, since the release of AcCho from 4-day denervated diaphragms was not diminished by either AH5183 or quinacrine. The spontaneous release of AcCho from the motor nerve terminals is highly sensitive to low concentrations of specific inhibitors and isprobably mediated by a carrier. Spontaneous release is apparently due to the incorporation into the membrane of the nerve terminal during exocytosis of the vesicular transport system responsible for moving AcCho into the vesicle.