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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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