Aggression in rainbow trout is inhibited by both MR and GR antagonists.
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) in combination with cortisol, the MR antagonist spironolactone (SA) in combination with cortisol or both antagonists in combination with cortisol. Aggressive behaviour was then assessed 1h subsequent to feeding. Our results showed that the attack latency was increased by exogenous cortisol, an effect that was not abolished by the antagonists. The intensity of aggression was not changed by exogenous cortisol. However, the intensity of aggression was significantly reduced by both antagonists. These results are discussed with regard to cortisol affecting aggressive behaviour through genomic and non-genomic pathways. Our results have demonstrated the involvement of both MR and GR in regulating behavioural responses during social interactions in teleost fish. The intensity of aggression seen in control and cortisol treated fish is probably mediated by the basal levels of cortisol through the intracellular MRs and GRs. We conclude that the initiative to engage in social confrontations is mediated through a non-genomic pathway, which could involve extracellular corticoid receptors. 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.
Schjolden
J
J
Department of Basic Sciences and Aquatic Medicine, Norwegian School of Veterinary Science, P.O. Box 8146 Dep, Ullevålsveien 72, N-0033, Oslo, Norway. joachim.schjolden@veths.no
Basic
D
D
Winberg
S
S
D000374:Aggression / Q000187:drug effects*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects; D004338:Drug Combinations; D057075:Enzyme Assays / Q000379:methods; D006727:Hormone Antagonists / Q000494:pharmacology*; D006854:Hydrocortisone / Q000097:blood / Q000494:pharmacology; D007398:Interpersonal Relations; D015735:Mifepristone / Q000494:pharmacology; D000451:Mineralocorticoid Receptor Antagonists; D017686:Oncorhynchus mykiss / Q000502:physiology*; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors* / Q000502:physiology; D018161:Receptors, Mineralocorticoid / Q000502:physiology; D013148:Spironolactone / Q000494:pharmacology; D018709:Statistics, Nonparametric; D014741:Video Recording / Q000379:methods
D000893:Anti-Inflammatory Agents; D004338:Drug Combinations; D006727:Hormone Antagonists; D000451:Mineralocorticoid Receptor Antagonists; D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D013148:Spironolactone; D015735:Mifepristone; D006854:Hydrocortisone