Adverse events during early developmental stages can induce persistent changes in central stress circuits, leading to increased stress sensitivity in adulthood, as is apparent in the maternally separated (MS) rat model. It is widely accepted that the stress peptide corticotropin-releasing factor (CRF) by binding to CRF1 and 2 receptors (CRFR1 and CRFR2) is key to these phenotypic changes.