A substantial body of research has suggested the possible role of dopamine (DA) dysfunctions in mood disorders: (a) levels of DA are decreased, D2 receptor binding in the striatum is increased, and striatal DA transporter is increased in depression; (b) different DA receptors, mostly D1–D2 heterodimers, and their distribution in different brain region have been suggested to be involved in the etiology of depression; (c) mesolimbic DA neurons could be linked to some nuclear symptoms of depression, such as loss of motivation and motor retardation [13,14]. This evidence concerns the gene SLC6A3 and depressive symptom measurement.