Serotonin (5-hydroxytryptamine, 5HT) is a biologically active amine present both, in the brain and the periphery, where it has different physiological functions. 5HT also regulates brain development and development of its own neurons during prenatal period. Alterations in the system that regulates metabolism and function of 5HT could be one of the possible biological basis of behavioral disordes that include autism. High concentrations of serotonin in blood is one of the most common physiological symptoms in persons with autism. It is assumed that high 5HT concentrations present in blood during fetal and early postnatal development can inhibit growth and development of 5HT neurons and lead to anatomical and functional changes in the brain. In order to examine the effects oh high levels of 5HT during the prenatal development on 5HT-related gene expression in the central and peripheral 5HT compartments, one group of rats was treated with serotonin precursor (5HTP, 25 mg/kg), and another group with non-selective inhibitor of monoamine-oxidase (TCP, 2 mg/kg), from gestational day 13 to postnatal day 21. The control group was treated with saline solution in the same manner. In this study I examined the impact of these treatments on the expression of genes for tryptophan hydroxylase (Tph 1 i 2) and monoamine oxidase (Mao A). Treatments with 5HTP and TCP did not cause statistically significant alterations in gene expression of Tph 1 and Mao A in the periphery. In the central compartment I observed decreased serotonin metabolism in the group treated with serotonin precursor (5HTP) and in the group treated with monoamine-oxidase inhibitor (TCP). I detected a significant decrease in Mao A gene expression and indicative decrease in Tph 2 gene expression. The results suggest that the perinatal treatments with 5-hydroxytriptophan and tranylcypromine have induced long-lasting compensatory changes in the expression of genes involved in 5HT metabolism.