Dopamine (DA) transmission plays a key role in reward, motivation, and action selection, and becomes dysregulated in substance-use disorders and Parkinson’s disease. Midbrain DA neurons form vast axonal arbours in the striatum, presenting opportunities for local axonal regulation of DA signalling by diverse interacting mechanisms. Striatal DA transporters (DATs) and γ-aminobutyric acid receptors (GABA-Rs) are both thought to limit DA axon activation and thereby attenuate DA release probability whilst also supporting the frequency-dependence of DA release. We tested whether these convergent mechanisms might interact, and potentially co-operate, to regulate DA release. We detected DA release using fast-scan cyclic voltammetry and are assessing DA axon membrane potential using the newly developed genetically-encoded voltage sensor ASAP5f in mouse dorsal and ventral striatum in acute slices. We found that GABAA+B-R antagonists, bicuculline and CGP-55845, reduced the effect of DAT inhibitor cocaine on DA release. This interaction was independent of any recruitment of D1- or D2-DA receptors, suggesting it does not require indirect effects of elevated DA on wider striatal circuitry, but was mediated by interacting mechanisms directly on DA axons. We explored a role for G-protein-coupled inwardly-rectifying K+ (GIRK) channels and found that GIRK inhibition alters the control of DA release by DATs and GABA-Rs. These data suggest a co-operation between DATs and GABA-Rs in shaping striatal DA release that involves GIRK channels. Imaging of the voltage sensor ASAP5f expressed in DA axons is underway to identify how DATs, GABA-Rs and GIRK channels together shape the axonal excitability that underlies DA release.