Neural mechanisms of modulations of empathy and altruism by beliefs of others' pain
Abstract
Perceived cues signaling others' pain induce empathy which in turn motivates altruistic behavior toward those who appear suffering. This perception-emotion-behavior reactivity is the core of human altruism but does not always occur in real life situations. Here, by integrating behavioral and multimodal neuroimaging measures, we investigate neural mechanisms underlying modulations of empathy and altruistic behavior by beliefs of others' pain. We show evidence that lack of beliefs of others' pain reduces subjective estimation of others' painful feelings and decreases monetary donations to those who show pain expressions. Moreover, lack of beliefs of others' pain attenuates neural responses to their pain expressions within 200 ms after face onset and modulates neural responses to others' pain in the insular, post-central, and frontal cortices. Our findings suggest that beliefs of others’ pain provide a cognitive basis of human empathy and altruism and unravel the intermediate neural mechanisms.
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Source data files have been provided for Figures 1-6 and Appdendix 1 Figure 1.
Article and author information
Author details
Funding
Ministry of Science and Technology of China (2019YFA0707103)
- Shihui Han
Natural Science Foundation of China (31871134)
- Shihui Han
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: This study was approved by the local Research Ethics Committee of the School of Psychological and Cognitive Sciences, Peking University. All participants provided written informed consent after the experimental procedure had been fully explained. Participants were reminded of their right to withdraw at any time during the study.
Copyright
© 2021, Yu & Han
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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