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Program & Abstract Book - EPFL Latsis Symposium 2009

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<strong>EPFL</strong> <strong>Latsis</strong> <strong>Symposium</strong> <strong>2009</strong>: Understanding Violence<br />

S-7<br />

32<br />

February 11-13 <strong>2009</strong><br />

ty p e s o f a g g r e s s i o n a n D t y p e s o f b r a i n<br />

m e c h a n i s m s . th e r o l e o f g l u c o c o r t i c o i D s<br />

Haller, Joseph<br />

Behavioural Neurobiology Department Institute of Experimental<br />

Medicine Budapest, Hungary<br />

Aggression is a behavioral mechanism of competition, which consists of acts<br />

that are aimed at or threat with, inflicting physical harm in social conflict.<br />

Aggressiveness is expressed by all species that are endowed with appropriate<br />

motor skills and neural systems. As such, this behavior cannot be considered<br />

abnormal per se. Yet, aggressiveness constitutes a major problem<br />

in human societies. Those manifestations of aggression that raise the largest<br />

concerns either loose their competitive role (they are internally driven<br />

rather than goal oriented) or disregard social rules, for which reasons they<br />

cannot be considered normal any more. Not surprisingly, such abnormal<br />

manifestations of aggressiveness usually occur in the context of various<br />

psychological disorders.<br />

We argue here that the neural control of normal and abnormal aggression<br />

is different, and changes in glucocorticoid secretion patterns are among the<br />

factors that underlie the behavioral and neural shifts that lead to abnormal<br />

aggression. This proposal will be substantiated by laboratory studies<br />

involving models of abnormal aggression. We will show that factors that<br />

lead to psychopathology-associated abnormal aggression in humans result<br />

in the development of abnormal aggression patterns in laboratory rodents.<br />

Among the eliciting factors, the ones that affect glucocorticoid secretion<br />

will be in focus. We will also show that the neural control of such abnormal<br />

aggression patterns is different from the one that underlies male rivalry aggression,<br />

which can be considered normal in laboratory rodents. Important<br />

differences were found at many levels of the neuronal circuitry that controls<br />

aggression, e.g. in the prefrontal cortex, septum, extended amygdala,<br />

hypothalamus, and brainstem. We will also show that normal and abnormal<br />

aggression responds differently to pharmacological agents, suggesting that<br />

agents that decrease rivalry aggression will not necessarily decrease abnormal<br />

manifestations of aggressiveness. We suggest that different types of<br />

human aggression need different pharmacological approaches.<br />

Our findings demonstrate that aggression is not a unitary phenomenon,<br />

neither in terms of behavioral manifestations nor in terms of neural control.<br />

A differentiated view on these phenomena offers the chance of a deeper<br />

understanding and may enable the development more efficient treatment<br />

strategies.

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