title: The amygdala and autism: implications from non-human primate studies.
abstract: Brothers (1990) has proposed that the amygdala is an important component of the neural network that underlies social behavior. Kemper and Bauman (1993) identified neuropathology in the amygdala of the postmortem autistic brain. These findings, along with recent functional neuroimaging data, have led Baron-Cohen et al. (2000) to propose that dysfunction of the amygdala may be responsible, in part, for the impairment of social behavior that is a hallmark feature of autism. Recent data from studies in our laboratory on the effects of amygdala lesions in the adult and infant macaque monkey do not support a fundamental role for the amygdala in social behavior. If the amygdala is not essential for the component processes of social behavior, as seems to be case in both non-human primates and selected patients with bilateral amygdala damage, then it is unlikely to be the primary substrate for the impaired social behavior of autism. However, damage to the amygdala does have an effect on a monkey's response to normally fear-inducing stimuli, such as snakes, and removes a natural reluctance to engage novel conspecifics in social interactions. These findings lead to the conclusion that an important role for the amygdala is in the detection of threats and mobilizing an appropriate behavioral response, part of which is fear. Interestingly, an important comorbid feature of autism is anxiety (Muris et al. 1998). If the amygdala is pathological in subjects with autism, it may contribute to their abnormal fears and increased anxiety rather than their abnormal social behavior.
authors: Department of Psychiatry and Behavioral Sciences and Center for Neuroscience, The M.I.N.D. Institute, University of California at Davis, Davis, CA 95817, USA. dgamaral@ucdavis.edu
authors: D G
authors: DG
authors: Amaral
authors: M D
authors: MD
authors: Bauman
authors: C Mills
authors: CM
authors: Schumann
mesh_terms: D000679:Amygdala / Q000293:injuries / Q000503:physiopathology*; D000818:Animals; D001321:Autistic Disorder / Q000209:etiology / Q000503:physiopathology*; D001925:Brain Damage, Chronic / Q000150:complications / Q000503:physiopathology*; D001931:Brain Mapping; D004195:Disease Models, Animal; D000882:Haplorhini; D006801:Humans