Dopamine releasing neurons in the substantia nigra pars compacta inhibit target cells in the striatum through postsynaptic activation of γ-aminobutyric acid (GABA) receptors. However, the molecular mechanisms responsible for GABAergic signaling remains unknown. This study found that inhibitory co-transmission from midbrain dopaminergic neurons does not depend on cell-autonomous GABA synthesis, but instead on presynaptic import from the extracellular space through the membrane transporter Gat1. The Gat1 knockout mice were generated by homologous recombination in mouse embryonic stem cells. The dataset includes electrophysiology, fiber photometry, and immunohistochemistry data.