SLC6A3 and attention deficit-hyperactivity disorder: In the zebrafish model, the loss of adgrl3 leads to a reduction of dopaminergic neurons in the ventral diencephalon and a hyperactive/impulsive phenotype [23], whereas in Adgrl3-knockout mice, an increase in reward motivation and activity level as well as other ADHD-analogous behaviors was observed—parallel to dysregulation of the dopamine transporter [24, 25].