In conclusion, our finding that different types of voltage-gated Ca2+ channels can compensate each other, modulate SN DA activity-patterns, and serve as alternative Ca2+ sources for the same downstream signalling pathway (NCS-1/D2-AR/GIRK2) that is inhibiting the electrical activity of SN DA neurons in a dopamine-dependent fashion, provides new insights into flexible age- and calcium-dependent activity-control of SN DA neurons, that might need to be considered for LTCC-based drug therapy of PD and beyond. Here, NCS1 is linked to Parkinson disease.