During the first three postnatal weeks, the levels of tryptophan in the brain are exceptionally high, 2--4 times those found in adult rats. This is related to two main peculiarities concerning tryptophan transport in young animals: 1. the lack of tryptophan binding onto serum albumin which makes its diffusion from plasma to tissues easier for the early life period; 2. the greater capacity of synaptosomes from neonates to accumulate tryptophan. Experiments consisting of electrolytic lesioning of the midbrain raphé or 5, 7-dihydroxytryptamine treatment clearly demonstrate that the uptake or tryptophan during postnatal development is not more active in serotoninergic than in other types of nerve terminals. In adult rats, changing the concentration of tryptophan induces parallel modifications in the rate of 5-HT synthesis in the brain since the rate limiting enzyme, tryptophan hydroxylase, is not saturated by its substrate. In contrast, neither tryptophan loading, nor parachlorophenylalanine administration (resulting in a marked decrease in brain tryptophan levels) alters the rate of 5-HT synthesis in the CNS of neonates, indicating that tryptophan hydroxylase is saturated during the early life period. These results are discussed in relation to the possible non-transmitter role of 5-HT during brain growth.