THE mechanism of the effects of large doses of L-dopa on brain function is ill-defined. This form of precursor loading produces marked increases in brain dopamine, little or no change in noradrenaline, and a substantial decrease in serotonin with an initial increase in 5-H indolyl-3-acetic acid (5-HIAA)^1–3. These observations suggest that serotonin may be released by L-dopa or its metabolites. Isolated synaptosomes (pinched-off nerve endings) actively accumulate exogenously labelled amines into structures which normally contain these amines^4–6. Although the distribution of the labelled amine in the endogenous stores is not clearly defined, these structures seem to provide valid models for nerve endings in brain and may afford a direct and sensitive means of assessing the influence of drugs on the release of neurohumours. Using this technique, we have found that L-dopa profoundly affects the efflux of cerebral monoamines.