The amygdala is widely known to be involved in the appraisal of emotion, registration of fear, and social functioning. This article adds relevant research to the theory that abnormality in the amygdala may be necessary for clinical autism. Indeed, the paper introduces necessary background on the role of the social brain and autism. For instance, it mentions experiments that utilize functional MRI to conclude that individuals with high-functioning autism have lower amygdala activation at the sight of human faces than the typically developing control group. In order to understand the later experiment, it is crucial to know the role of the amygdala and greater limbic system in social functioning. Thus, the article does an excellent job of preparing the reader for later data by providing the appropriate neurobiological context.
The methodology of this experiment involved introducing mature Rhesus monkeys with lesions to the amygdala in a clan of typically developing Rhesus monkeys. The results concluded that those with amygdala lesions were more outgoing in social interaction (grooming, playing, etc.) than the control group. However, since this behavior was still present in both groups, the results do not support the claim that the amygdala is a key contributor to social dysfunction in autism spectrum disorder (ASD).
A critique of this paper involves the nature of the experiment. Since only mature monkeys were used, it is unclear whether abnormal functioning in the amygdala is translatable to ASD in the adolescent phase; ASD behaviors in humans are likely to be seen within the first few years of birth. Since the organization of the brain is highly malleable at such age, a brain with an abnormally functioning amygdala is different than one without its functioning entirely. Additionally, a limitation of the experiment involves using Rhesus monkeys since humans with amygdala lesions are scarce. Though social behavior in a clan of Rhesus monkeys may resemble that of human interaction, it is difficult to say that pro-sociality of the experimental group is synonymous to the day-to-day experience of emotion and communication of a human.
It is clear that this article presents a genuine contribution to the neuroscience of ASD. The results of this experiment favor a widespread network that is affected in the clinical display of ASD and not just the amygdala or one part of the brain. It is more likely that an entire system of moving parts is involved in the registration of faces, words, and generation of a response in human social interaction. Thus, the brain of an individual with ASD is likely experiencing a variety of factors that contribute to the display of social functioning.