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The amygdala and autism: implications from non-human primate studies
Open accessAbstract
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.
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“This same reasoning applies just as well to explanations for anxiety: reduced modulation of limbic activity via higher cortical systems may result in chronic, unchecked perception of threat and subsequent anxiety (Amaral et al., 2003).”
From Sensory, emotional and cognitive contributions to anxiety in autism spectrum disorders (2017) · cites this paper as Amaral et al., 2003
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Metadata
- Authors
- Amaral, D. G., Bauman, M. D., & Mills Schumann, C.
- Affiliations
- University of California, Davis (US)
- Corresponding author
- Amaral, D. G.
- Venue
- Genes, Brain and Behavior
- Publisher
- Wiley
- Published
- 2003-10
- Volume
- 2
- Issue
- 5
- Pages
- 295-302
- ISSN
- 1601-183X (ISSN-L)
- 1601-1848
- OpenAlex
- W1561508305
- Cited by
- 184
- References
- 66
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 16 · 2023: 2 · 2022: 6 · 2021: 5 · 2020: 8 · 2019: 9 · 2018: 1 · 2017: 11 · 2016: 6 · 2015: 5 · 2014: 11 · 2013: 7 · 2012: 15
- FWCI
- 1.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes Brain & Behavior (publishedVersion)
- PubMed (publishedVersion)
- Funders
- John D. and Catherine T. MacArthur Foundation
- National Institutes of Health
- National Institute of Mental Health (R01MH057502)
- National Center for Research Resources (P51RR000169, RR-00169)
- California National Primate Research Center (RR00169)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Face Recognition and Perception
- Keywords
- amygdala, autism spectrum disorder, social behavior, amygdala lesions, macaque, fear, threat detection, anxiety, social interaction, autism comorbidity
- MeSH terms
- Amygdala, Animals, Haplorhini, Autistic Disorder, Brain Damage, Chronic, Brain Mapping, Disease Models, Animal, Humans
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