SUMMARY1. Transmission of a single nerve impulse has been investigated at the nerveelectroplaque junction of Torpedo marmorata in the presence of 4-aminopyridine (4-AP), a drug which powerfully potentiates evoked transmitter release.2. Three methodological approaches were used conjointly. These were (i) electrophysiological recording of the compound electroplaque potential (e.p.p.), (ii) radiochemical measurement of evoked acetylcholine (ACh) release and (iii) analysis of the content of ACh and ATP in the tissue at brief time intervals during the course of the e.p.p. and soon after. The last was achieved by using a stimulator coupled to a rapid tissue freezer.3. In the response to a single stimulus, 4-AP enhanced in a dose-dependent manner the size of the e.p.p., increasing the duration much more than the amplitude. At

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The metabolism of acetate was investigated in the nerve-electroplaque system of Torpedo marmorata. In intact fragments of electric organ, radiolabeled acetate was incorporated into acetylcholine (ACh), acetylcarnitine (ACar), and three amino acids: aspartate, glutamate, and glutamine. These compounds were identified by TLC, high-voltage electrophoresis, column chromatography, and enzymic tests. The system responsible for acetate transport and incorporation into ACh displayed a higher affinity but a lower Vmax than that involved in the synthesis of ACar and amino acids. Choline, when added to the medium, increased the rate of acetate incorporation into ACh but decreased (at concentrations greater than 10(-5) M) that into ACar and amino acids. Monofluoroacetate slightly depressed ACh and ACar synthesis from external acetate but inhibited much more the synthesis of amino acids. During repetitive nerve stimulation, the level of the newly synthetized [14C]ACh was found to oscillate together with that of endogenous ACh, but the level of neither [14C]ACar nor the 14C-labeled amino acids exhibited any significant change as a function of time. This means that there is probably no periodic transfer of acetyl groups between ACh and the investigated metabolites in the course of activity. Acetate metabolism was also tested in the electric lobe (which contains the cell bodies of the neurons innervating the electric organ) and in Torpedo synaptosomes (which are nerve terminals isolated from the same neurons). Radioactive pyruvate and glutamine were also assayed in some experiments for comparison with acetate. These observations are discussed in connection with ACh metabolism under resting and active conditions in tissues where acetate is the preferred precursor of the neurotransmitter.

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