Release of Monoamines Evoked by Field Stimulation– Studies on Some Ionic and Metabolic Requirements

Electrical field stimulation of isolated tissues can cause release of 3 H‐monoamines previously taken up into monoamine nerve terminals. The stimulation‐induced overflow of tritium was investigated in isolated irides previously incubated with 3 H‐noradrenaline, cerebral cortex slices incubated with 3 H‐noradrenaline or 3 H‐5‐hydroxytryptamine and neostriatal slices incubated with 3 H‐dopamine. No stimulation‐induced tritium overflow was obtained if Ca ++ was excluded from the buffer or tetrodotoxin was added to the buffer. Mg ++ 20 mM completely inhibited the stimulation‐induced overflow from isolated rat iris. Exclusion of K + slightly increased the stimulation‐induced overflow. At K + 20 mM no stimulation‐induced overflow was obtained. K + 50 mM evoked a great increase of the tritium overflow. Low Na + concentrations reduced the stimulation‐induced overflow. In agreement with previous investigations it is concluded that the present stimulation technique may cause relase of monoamines via action potentials propagated along the nerves. Inhibition of oxidative phosphorylation moderately increased the stimulation‐induced overflow from the rat iris. This is probably due to partial inhibition of noradrenaline reuptake into the nerve terminals. Exclusion of glucose from the buffer greatly increased both the spontaneous and the stimulation‐induced tritium overflow. The stimulation‐induced overflow in the absence of glucose was only partially Ca ++ ‐dependent. It is concluded that the release process for noradrenaline is not immediately inhibited after interference with energy‐yielding processes.