Anthropomorphizing without Social Cues Requires the Basolateral Amygdala
Abstract
Anthropomorphism, the attribution of distinctively human mental characteristics to nonhuman animals and objects, illustrates the human propensity for extending social cognition beyond typical social targets. Yet, its processing components remain challenging to study because they are typically all engaged simultaneously. Across one pilot study and one focal study, we tested three rare people with basolateral amygdala lesions to dissociate two specific processing components: those triggered by attention to social cues (e.g., seeing a face) and those triggered by endogenous semantic knowledge (e.g., imbuing a machine with animacy). A pilot study demonstrated that, like neurologically intact control group participants, the three amygdala-damaged participants produced anthropomorphic descriptions for highly socially salient stimuli but not for stimuli lacking clear social cues. A focal study found that the three amygdala participants could anthropomorphize animate and living entities normally, but anthropomorphized inanimate stimuli less than control participants. Yet, amygdala participants could anthropomorphize across all stimuli when explicitly questioned, demonstrating that the ability to make social attributions as such is intact. Our findings suggest that the amygdala contributes to how we anthropomorphize stimuli that are not explicitly social.
Additional Information
© 2018 Massachusetts Institute of Technology. Posted Online December 18, 2018. We dedicate this article to the memory of John Cacioppo, who passed away while the article was being finalized and whose seminal work in social neuroscience guided the questions and approaches we present here. German comparison participants were recruited by Tania Singer. R. H. was supported by the German Research Foundation (DFG) BE 5465/2-1 and HU 1302/4-1. R. A. and L. K. P. were supported by a Conte Center from NIMH (P50MH094258).Attached Files
Published - jocn_a_01365.pdf
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Additional details
- Eprint ID
- 91963
- Resolver ID
- CaltechAUTHORS:20190102-074401938
- Deutsche Forschungsgemeinschaft (DFG)
- BE 5465/2-1
- Deutsche Forschungsgemeinschaft (DFG)
- HU 1302/4-1
- NIH
- P50MH094258
- Created
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2019-01-02Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field