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First published online November 17, 2006
Journal of Experimental Biology 209, 4581-4589 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02565
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Interactions between the neural regulation of stress and aggression

Cliff H. Summers1,2,* and Svante Winberg3,4

1 Department of Biology, University of South Dakota, Vermillion, SD 57069 USA
2 Neuroscience Group, Division of Basic Biomedical Sciences, University of South Dakota School of Medicine, Vermillion, SD 57069, USA
3 Department of Basic Science and Aquatic Medicine, Norwegian School of Veterinary Science, PO Box 8146, N-0033 Oslo, Norway
4 Department of Comparative Physiology, Evolutionary Biology Centre, Uppsala University, Norbyvägen 18A, SE-752 36 Uppsala, Sweden


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  		Fig. 1. The development of an aggressive social interaction over time progresses through distinct stages of neuroendocrine and behavioral state. In the first phase, prior to interaction baseline levels of plasma glucocorticoids (B=corticosterone in lizards, rats, mice, frogs, birds; F=cortisol in fish, humans, sheep, hamsters) and serotonergic and perhaps dopaminergic activity in brain regions associated with aggression and motivation influence the animal's predisposition (positively or negatively) toward aggression. The prefight neuroendocrine profile is distinctly different in individuals that will become dominant (dom), and those that will become subordinate (sub). At some point, when combatants meet and social engagement begins, early social signals and rapid changes in neuroendocrine profile of putatively dominant individuals generate motivation toward behavior. No aggression has occurred yet, but increased activity of glucocorticoids, serotonin (5-HT) and dopamine (DA) enhance the likelihood of heightened behavioral interaction, culminating in aggression. After aggression begins, both animals are fully responsive to stress, and expressing social signals. Aggression is very stressful, and for that reason, serotonergic and glucocorticoid activities rise dramatically and rapidly in animals that become dominant and those that become subordinate. Surprisingly neither elevated plasma glucocorticoid levels nor serotonergic activity inhibit aggression at this time. Glucocorticoids appear to be necessary for the full expression of early aggression, and elevated B or F plus increased serotonergic activity appear to passively allow aggression. Finally, after social rank is established, chronically elevated or applied 5-HT and glucocorticoids inhibit aggression. Chronic neuroendocrine state likely influences subsequent interactions.

 




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