Program & Abstract Book - EPFL Latsis Symposium 2009

EPFL Latsis Symposium 2009: Understanding Violence
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Abstracts for Speakers
ne u r o g e n e t i c a n D n e u r o h o r m o n a l m e c h a -
n i s m s o f p r o s o c i a l a n D a g g r e s s i v e b e h a v i o r
Meyer -Lindenberg, Andreas
Central Institute of Mental Health, Mannheim, Germany
Well-being and survival in primates, including humans, depends critically
on social interactions, and disturbed social behavior is a key component of
diseases such as autism, schizophrenia, and anxiety disorders. However,
little is known about specific neurobiological factors shaping the human social
brain. Since many aspects of social function are highly heritable (4), we
have adopted a genetic approach to identify molecular and systems-level
mechanisms of social cognition in humans. Studies in Williams Syndrome, a
genetic condition with pronounced hypersociability, identified abnormal prefrontal
regulation of amygdala as a neural substrate of social fear regulation
under genetic control. Studies of candidate gene polymorphisms (5-HTTLPR,
MAOA vNTR) impacting on personality, aggressive behavior, and emotional
regulation modulate on similar circuitry. In animals, oxytocin and vasopressin
are key mediators of complex emotional and social behaviors, reduce
anxiety and impact on fear conditioning and extinction. Recently, oxytocin
administration in humans was shown to increase trust, suggesting involvement
of the amygdala, a central component of the neurocircuitry of fear and
social cognition that has been linked to trust and highly expresses oxytocin
receptors in many mammals. We report on functional neuroimaging studies
in healthy human subjects. In males receiving oxytocin or placebo, oxytocin
potently reduced activation of the amygdala and reduced coupling of
the amygdala to brainstem regions implicated in autonomic and behavioral
manifestations of fear. We also report on imaging genetic studies characterizing
the effects of genetic variation in the vasopressin receptor (AVPR1A)
and the oxytocin receptor gene (OXTR), implicated in risk for autism, on
brain structure and function related to emotional regulation and social behavior.
Taken together, the results suggest neural mechanisms for social
cognition in the human brain that begin to define mechanisms for both pro-
and antisocial behavior as well as molecular approaches to modulate and
treat these behaviors.
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