The causal role of the somatosensory cortex in prosocial behaviour
- Netherlands Institute for Neuroscience, Netherlands
- University of Bologna, Italy
Abstract
Witnessing another person's suffering elicits vicarious brain activity in areas active when we ourselves are in pain. Whether this activity influences prosocial behavior remains debated. Here participants witnessed a confederate express pain via a reaction of the swatted hand or via a facial expression and could decide to reduce that pain by donating money. Participants donate more money on trials in which the confederate expressed more pain. EEG shows that activity of the SI hand region explains variance in donation; TMS shows that altering this activity interferes with the pain-donation coupling only when pain is expressed by the hand and HD-tDCS that altering SI activity also interferes with pain perception. These experiments show vicarious somatosensory activations contribute to prosocial decision-making and suggest they do so by helping transform observed reactions of affected body-parts into accurate perceptions of pain that are necessary for decision making.
Data availability
fMRI and EEG data have been deposited in Zenodo. Source data files have been provided for all figures
-
The causal role of the somatosensory cortex in prosocial behavior - Pain LocalizerPublicly available at Zenodo.
-
The causal role of the somatosensory cortex in prosocial behavior - EEG datasetPublicly available at Zenodo.
Article and author information
Author details
Mario Carlo Severo
Funding
Nederlandse Organisatie voor Wetenschappelijk Onderzoek (VIDI: 452-14-015)
- Valeria Gazzola
Brain and Behavior Research Foundation (NARSAD young investigator 22453)
- Valeria Gazzola
H2020 European Research Council (ERC-StG-312511)
- Christian Keysers
Cogito Foundation (R-117/13)
- Alessio Avenanti
Fundação Bial (298/16)
- Alessio Avenanti
Cogito Foundation (14-139-R)
- Alessio Avenanti
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: All studies have been approved by the Ethics Committee of the University of Amsterdam, the Netherlands.Project identifiers:2016-BC-73942016-BC-71302016-PSY-64852014-EXT-34762014-EXT-3432All participants received monetary compensation and gave their informed consent for participation in the study.
Copyright
© 2018, Gallo et al.
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.
Metrics
-
- 5,561
- views
-
- 745
- downloads
-
- 71
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
A two-part list of links to download the article, or parts of the article, in various formats.
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
The causal role of the somatosensory cortex in prosocial behaviour
eLife 7:e32740.
https://doi.org/10.7554/eLife.32740
Further reading
-
- Cell Biology
- Neuroscience
Experience shapes the brain as neural circuits can be modified by neural stimulation or the lack of it. The molecular mechanisms underlying structural circuit plasticity and how plasticity modifies behaviour are poorly understood. Subjective experience requires dopamine, a neuromodulator that assigns a value to stimuli, and it also controls behaviour, including locomotion, learning, and memory. In Drosophila, Toll receptors are ideally placed to translate experience into structural brain change. Toll-6 is expressed in dopaminergic neurons (DANs), raising the intriguing possibility that Toll-6 could regulate structural plasticity in dopaminergic circuits. Drosophila neurotrophin-2 (DNT-2) is the ligand for Toll-6 and Kek-6, but whether it is required for circuit structural plasticity was unknown. Here, we show that DNT-2-expressing neurons connect with DANs, and they modulate each other. Loss of function for DNT-2 or its receptors Toll-6 and kinase-less Trk-like kek-6 caused DAN and synapse loss, impaired dendrite growth and connectivity, decreased synaptic sites, and caused locomotion deficits. In contrast, over-expressed DNT-2 increased DAN cell number, dendrite complexity, and promoted synaptogenesis. Neuronal activity modified DNT-2, increased synaptogenesis in DNT-2-positive neurons and DANs, and over-expression of DNT-2 did too. Altering the levels of DNT-2 or Toll-6 also modified dopamine-dependent behaviours, including locomotion and long-term memory. To conclude, a feedback loop involving dopamine and DNT-2 highlighted the circuits engaged, and DNT-2 with Toll-6 and Kek-6 induced structural plasticity in this circuit modifying brain function and behaviour.
-
- Cell Biology
- Neuroscience
Sorting nexin 4 (SNX4) is an evolutionary conserved organizer of membrane recycling. In neurons, SNX4 accumulates in synapses, but how SNX4 affects synapse function remains unknown. We generated a conditional SNX4 knock-out mouse model and report that SNX4 cKO synapses show enhanced neurotransmission during train stimulation, while the first evoked EPSC was normal. SNX4 depletion did not affect vesicle recycling, basic autophagic flux, or the levels and localization of SNARE-protein VAMP2/synaptobrevin-2. However, SNX4 depletion affected synapse ultrastructure: an increase in docked synaptic vesicles at the active zone, while the overall vesicle number was normal, and a decreased active zone length. These effects together lead to a substantially increased density of docked vesicles per release site. In conclusion, SNX4 is a negative regulator of synaptic vesicle docking and release. These findings suggest a role for SNX4 in synaptic vesicle recruitment at the active zone.
