Daily injection of L-triiodothyronine (10 μg/100 g, s.c.) for 30 days to neonatal rats significantly enhanced the metabolism of 5-hydroxytryptamine as reflected by increased tryptophan hydroxylase activity and 5-hydroxyindoleacetic acid levels of certain discrete brain regions. However, neonatal L-triiodothyronine treatment produced no change in <sup>3</sup>H-5-hy-droxytryptamine uptake by crude synaptosomes. Chronic treatment with apomorphine (1 mg/ kg/day, s.c.) for 15 days, beginning from 15 days of age, increased tryptophan hydroxylase activity as well as 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels and blocked the uptake of <sup>3</sup>H-labelled serotonin in crude synaptosomes of normal and L-triiodothyronine-treated animals. Furthermore, apomorphine (which is known to indirectly stimulate 5-hy-droxytryptaminergic neurons) produced a greater increase in tryptophan hydroxylase and 5-hydroxyindoleacetic acid in the mid-brain region of neonatally hyperthyroid animals as compared to normal rats. These data indicate that excess thyroid hormone in early life not only increases the turnover of brain 5-hydroxytryptamine, but also enhances the sensitivity of dopamine receptor sites, thus amplifying the stimulating action of apomorphine. Our findings also suggest that thyroid hormone in early life advances the overall development of monoaminergic systems in the brain.