Francesca Vitale, Mabel Urrutia, Alessio Avenanti, Manuel de Vega
{"title":"You are fired! Exclusion words induce corticospinal modulations associated with vicarious pain.","authors":"Francesca Vitale, Mabel Urrutia, Alessio Avenanti, Manuel de Vega","doi":"10.1093/scan/nsad033","DOIUrl":null,"url":null,"abstract":"<p><p>Self- and vicarious experience of physical pain induces inhibition of the motor cortex (M1). Experience of social rejections recruits the same neural network as physical pain; however, whether social pain modulates M1 corticospinal excitability remains unclear. This study examines for the first time whether social exclusion words, rather than simulated social exclusion tasks, modulate embodied sensorimotor networks during the vicarious experience of others' pain. Participants observed visual sequences of painful and functional events ending with a superimposed word with social exclusion, social inclusion or non-social meaning. Motor-evoked potentials (MEPs) to single-pulse transcranial magnetic stimulation of the left M1 were recorded at 400 or 550 ms from word onset. MEPs tended to inhibit during the observation of pain, relative to functional events. Moreover, MEPs recorded at 400 ms from word onset, during pain movies, decreased following the presentation of exclusion, relative to inclusion/neutral words. The magnitude of these two modulations marginally correlated with participants' interindividual differences in personal distress and self-esteem. These findings provide evidence of vicarious responses to others' pain in the M1 corticospinal system and enhancement of such vicarious response in the earlier phases of semantic processing of exclusion words-supporting activation of social pain-embodied representations.</p>","PeriodicalId":21789,"journal":{"name":"Social cognitive and affective neuroscience","volume":null,"pages":null},"PeriodicalIF":3.9000,"publicationDate":"2023-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b3/25/nsad033.PMC10263475.pdf","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Social cognitive and affective neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/scan/nsad033","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 1
Abstract
Self- and vicarious experience of physical pain induces inhibition of the motor cortex (M1). Experience of social rejections recruits the same neural network as physical pain; however, whether social pain modulates M1 corticospinal excitability remains unclear. This study examines for the first time whether social exclusion words, rather than simulated social exclusion tasks, modulate embodied sensorimotor networks during the vicarious experience of others' pain. Participants observed visual sequences of painful and functional events ending with a superimposed word with social exclusion, social inclusion or non-social meaning. Motor-evoked potentials (MEPs) to single-pulse transcranial magnetic stimulation of the left M1 were recorded at 400 or 550 ms from word onset. MEPs tended to inhibit during the observation of pain, relative to functional events. Moreover, MEPs recorded at 400 ms from word onset, during pain movies, decreased following the presentation of exclusion, relative to inclusion/neutral words. The magnitude of these two modulations marginally correlated with participants' interindividual differences in personal distress and self-esteem. These findings provide evidence of vicarious responses to others' pain in the M1 corticospinal system and enhancement of such vicarious response in the earlier phases of semantic processing of exclusion words-supporting activation of social pain-embodied representations.
期刊介绍:
SCAN will consider research that uses neuroimaging (fMRI, MRI, PET, EEG, MEG), neuropsychological patient studies, animal lesion studies, single-cell recording, pharmacological perturbation, and transcranial magnetic stimulation. SCAN will also consider submissions that examine the mediational role of neural processes in linking social phenomena to physiological, neuroendocrine, immunological, developmental, and genetic processes. Additionally, SCAN will publish papers that address issues of mental and physical health as they relate to social and affective processes (e.g., autism, anxiety disorders, depression, stress, effects of child rearing) as long as cognitive neuroscience methods are used.