The effects of GH on various types of behaviour in fish are well documented although the underlying mechanisms are not fully understood. In rainbow trout, an involvement of the brain dopaminergic system in mediating the behavioural effects of GH has been indicated, as GH can alter the brain dopaminergic activity. To further examine the role of the dopaminergic system in the mediation of GH effects on locomotion and foraging, GH- and sham-implanted juvenile rainbow trout were injected with the selective D1 dopamine antagonist SCH23390 or vehicle. Swimming and feeding activity was then studied by direct observation. Brains were thereafter sampled and analysed for the content of serotonin, dopamine and their metabolites in the hypothalamus, optic tectum, cerebellum, telencephalon, and brain stem. GH increased swimming activity as well as feed intake, effects which were abolished by SCH23390. By itself, the antagonist did not affect behaviour, nor did it affect the brain monoamines. In contrast, treatment with GH, with or without SCH23390, decreased the content of the dopamine metabolite homovanillic acid (HVA) in the optic tectum and the cerebellum, as well as the serotonin content (5-HT) in the optic tectum. It is concluded that the D1 dopamine receptor of the dopaminergic system appears to be of importance in the mediation of the effects of GH on behaviour.