The present study has investigated the effect of exogenous cortisol on aggression in juvenile rainbow trout, along with the involvement of mineralocorticoid (MR) and glucocorticoid receptors (GR) mediating the effects of cortisol. Fish were fed pellets supplemented with cortisol, the GR antagonist mifepristone (RU486), the MR antagonist spironolactone (SA) or combinations of these substances. Our results showed that the initiative to engage in social confrontation was diminished by cortisol, an effect that was not abolished by the antagonists. Moreover, the intensity of aggression was not increased by exogenous cortisol. However, the intensity of aggression was reduced by both antagonists. These results are discussed with regard to cortisol affecting aggressive behaviour through genomic and non- genomic pathways. The escalated aggression seen in control and cortisol treated fish is probably mediated by the basal levels of cortisol through the intracellular MRs and GRs. Our results have also demonstrated the involvement of both MR and GR in regulating behavioural responses during social interactions in teleost fish. It seems likely that the initiative to engage in social confrontations is mediated through a non-genomic pathway. Further, the majority of arguments lean towards the MR and GR antagonists blocking the effect of cortisol on aggressive intensity through intracellular receptors. If this is the case, then it is probable that these two aspects of aggressive behaviour are based on different neuronal mechanisms.