Previous studies from our group showed that brain serotonin deficiency in rodents affects the early postnatal growth of the pups, triggering behavioral alterations and problems in social communication. We aim at understanding the causal link between low levels of brain serotonin and growth retardation and altered behavior in the early postnatal phase of development. To do this we are using a knockout rat model lacking TPH2, the main enzyme involved in the first step of serotonin synthesis in the brain.To tackle growth retardation, we monitored the pituitary activity of the pups at different ages after birth (P2, P7 and P14) using a proteomic approach. Overall, we only found minor differences between heterozygous and knockout animals in the same age groups, which however included growth factors and their signaling pathways. To further elucidate the mechanistic causes of postnatal growth retardation, we conducted rescue experiments. As expected, daily supplementation of pups with the serotonin precursor 5-HTP restored the serotonin levels in the brain of TPH2-deficient animals and also improved their growth. Furthermore, early postnatal chronic inhibition of MAO-A, the main enzyme responsible for monoamine metabolism, also rescued the weight loss in TPH2 KO rodents. This inhibition of the main monoamine degradation pathway resulted in an increase in dopamine, but not serotonin levels in the brain of TPH2-deficientr rats, suggesting dopamine as a potential downstream mediator of serotonergic signaling in controlling early postnatal growth.Our results reveal a new role for central serotonin in the earliest phases of postnatal life.