The involvement of the α2-AR in mood dysregulation is also indicated by its upregulation in several brain areas in patients with depression,9 as well as by preclinical data showing α2-AR gene knockout mice to show depression-like behavior that is not sensitive to tricyclic antidepressants.24 This finding is further supported by the data in the present study showing that α2-AR activation by dexmedetomidine in the early postpartum period decreased the presence of functional and mood deficits among patients with prenatal depression who were susceptible to PPD. This evidence concerns the gene ADORA2A and progressive pseudorheumatoid arthropathy of childhood.