Neonatal tryptophan depletion and corticosterone supplementation result in depressive-like abnormalities in adult male mice

Current rodent models of human depression suffer from limited construct and external validity whereby they disregard the nature-nurture interactive origin of the disease and are normally suited to inflexible conditions (e.g. single background strain). We developed a animal model reproducing several depressive-like features (symptoms) through the combination of reduced serotonin and environmental stress during the early stages of postnatal life (aetiology). We tested whether the adult mice thereon obtained exhibited behavioral and neurochemical alterations isomorphic to symptoms of human depression.