Dopamine neurons in the substantia nigra pars compacta inhibit striatal neurons via GABA co-release, despite lacking GABA-synthesizing enzymes. Using conditional deletion of Slc6a1, the study shows that GABA uptake via GAT1 is essential for co-transmission. GABA is then packaged into vesicles by VMAT2. Aldh1a1 deletion had no effect.
GABAergic inhibition by dopamine neurons requires GAT1-mediated uptake and VMAT2-dependent packaging. Aldh1a1 is not involved. Co-release is rescued by re-expression of GAT1 or GAD enzymes.
Slc6a1^flox/flox conditional Knockout mouse — genOway-developed, crossed with Dat^IRES‑Cre and additional recombinase or reporter lines
Dopamine neuron signaling, GABA co-transmission, basal ganglia, movement disorders, synaptic inhibition
Conditional Knockout using Dat^Cre, viral rescue of GAT1 or GAD67/GAD65, ChR2 optogenetics, whole-cell electrophysiology in striatum, functional validation via latency and amplitude shifts
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