1 Uptake of 5-hydroxytryptamine (5-HT) by rat platelets in plasma was very rapid and diffusion did not contribute significantly at substrate concentrations that did not saturate the active transport.2 Under conditions which allowed measurement of initial rates of uptake, kinetic analysis revealed a high affinity uptake mechanism for 5-HT (K(m) = 0.7 muM).3 Uptake of dopamine was relatively slow and involved a lower affinity (K(m) = 70 muM) active transport process. Diffusion contributed significantly at concentrations that did not saturate the active transport.4 5-HT competitively inhibited uptake of dopamine, and vice versa; K(i) values for both amines were similar to their respective K(m) values for uptake.5 Chlorimipramine, desmethylimipramine and benztropine were tested as uptake inhibitors. Each was equipotent against 5-HT and dopamine, although the absolute potency of the drugs varied greatly. Chlorimipramine was the most potent (K(i)## 100 nM), and kinetic analysis revealed that the inhibition was competitive against both 5-HT and dopamine.6 Similar results were obtained in studies with human platelets: K(m) values for 5-HT and dopamine were about 1 muM and 100 muM respectively. Activity profiles of inhibitors were also similar: each compound tested was equipotent against 5-HT and dopamine, and the two amines each competitively inhibited uptake of the other.7 We conclude that dopamine is actively transported by platelets via the 5-HT uptake mechanism, but with a much lower affinity. There is no high-affinity dopamine-specific mechanism corresponding to that in the corpus striatum. Consequently although platelets may be valid models of transport in 5-hydroxytryptaminergic neurones, they should not be regarded as models for the dopamine transport mechanism found in dopaminergic neurones.