Brain Process Found for Social Behavior

The study, conducted by researchers from the U.S. National Institute of Mental Health (NIMH; Bethesda, MD, USA; www.nimh.nih.gov), compared the brains of healthy participants to those with a genetic flaw, resulting in Williams syndrome, a rare illness that causes unique alterations in social behavior. This comparison enabled the scientists to both identify a brain circuit for social function in the healthy human brain, and find the precise manner in which it was affected by genetic changes in Williams syndrome.

Individuals with William syndrome, who are missing approximately 21 genes on chromosome seven, are very social and empathetic, even in circumstances that would induce anxiety and fear in healthy individuals. They experience increased anxiety that is nonsocial, such as phobias and excessive worrying.

The investigators utilized functional magnetic resonance imaging (fMRI) to evaluate the amygdala and structures associated with it in 13 individuals with Williams syndrome who have normal intelligence and compared them to healthy controls. They showed participants pictures of fearful or angry faces. These faces are known to activate the amygdala. The fMRI scans demonstrated significantly less activation of the amygdala in participants with Williams syndrome in response to social stimuli that might be responsible for their fearfulness in social interactions.

Investigators then showed the individuals pictures of threatening scenes that did not have any people of faces in them and therefore had no immediate social component. In striking contrast to the response faces, the amygdala response to threatening scenes was abnormally increased in participants with Williams syndrome, echoing their extreme nonsocial anxiety.

The researchers located three regions of the prefrontal cortex, situated in the front part of the brain, that have been implicated in decision-making, representation of social knowledge, and judgment: the medial, dorsolateral, and orbitofrontal cortex. The investigators discovered a fragile network by which these three areas control amygdala activity. In Williams syndrome, this delivery system was considerably abnormal, specifically in the orbito-frontal cortex. This region did not activate for either task and was not functionally linked to the amygdala, as it was in healthy controls. Instead, the researchers noted increased activity and linkage in the medial area, which is consistent with the high level of empathy seen by individuals with Williams syndrome.




Related Links:
National Institute of Mental Health