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Modification of the transport velocity of both the native neuronal and cloned presynaptic dopamine transporter (DAT) has been reported following activation/inhibition of second messenger system pathways. In order to identify the mechanism by which the functional activity of human DAT (hDAT) is regulated, we assessed the [³H]dopamine uptake kinetics, [³H]CFT binding characteristics, and, via immunofluorescent confocal microscopy, the cellular localization profiles of the hDAT expressed in both Sf9 and COS‐7 cells following modulation of protein kinase C (PKC)‐ and protein kinase A (PKA)‐dependent pathways. As with both native neuronal and cloned DATs, acute exposure of hDAT expressing Sf9 cells to the PKC activator PMA (1 μM), but not αPDD, reduced the V_max (∼1 pmol/min/10⁵ cells) for [³H]DA uptake by ∼40%, an effect which was blocked by the protein kinase inhibitor staurosporine …