Exclusion is a social phenomenon that reliably causes negative consequences for the excluded. From aggression to self-control failure, exclusion yields several maladaptive dividends. However, neuroscience research has peered inside the mechanics of exclusion’s effects, yielding many valuable insights. The chief contribution of the neuroscience of exclusion has been to uncover that social exclusion is truly painful. Social pain’s automatic components in the brainstem, anterior cingulate and insular cortices, are counterbalanced by the controlled, regulatory function of the prefrontal cortex. In this chapter, we draw from literatures on emotion regulation, self-affirmation, and mindfulness to suggest ways in which both automatic and controlled neural responses to social exclusion can be altered to promote functional responses. Such regulatory modifications can promote affiliative over aggressive behavioral responses, prevent self-regulatory failure, and reduce stress and inflammatory responses in the body’s periphery. Given the substantial impact of individual differences on neural responses to exclusionary threats, there exist ways in which these regulatory strategies can be tailored to individual personality profiles. We hope to detail how the neuroscience of exclusion has matured and is now poised to transition from descriptive research to prescriptive interventions.

Chester, D., Riva, P. (2016). Brain mechanisms to regulate negative reactions to social exclusion. In P. Riva, J. Eck (a cura di), Social exclusion: Psychological approaches to understanding and reducing its impact (pp. 251-273). New York, NY : Springer International Publishing [10.1007/978-3-319-33033-4_12].

Brain mechanisms to regulate negative reactions to social exclusion

RIVA, PAOLO
2016

Abstract

Exclusion is a social phenomenon that reliably causes negative consequences for the excluded. From aggression to self-control failure, exclusion yields several maladaptive dividends. However, neuroscience research has peered inside the mechanics of exclusion’s effects, yielding many valuable insights. The chief contribution of the neuroscience of exclusion has been to uncover that social exclusion is truly painful. Social pain’s automatic components in the brainstem, anterior cingulate and insular cortices, are counterbalanced by the controlled, regulatory function of the prefrontal cortex. In this chapter, we draw from literatures on emotion regulation, self-affirmation, and mindfulness to suggest ways in which both automatic and controlled neural responses to social exclusion can be altered to promote functional responses. Such regulatory modifications can promote affiliative over aggressive behavioral responses, prevent self-regulatory failure, and reduce stress and inflammatory responses in the body’s periphery. Given the substantial impact of individual differences on neural responses to exclusionary threats, there exist ways in which these regulatory strategies can be tailored to individual personality profiles. We hope to detail how the neuroscience of exclusion has matured and is now poised to transition from descriptive research to prescriptive interventions.
Capitolo o saggio
Affiliative responses; Aggressive responses; Automatic responses; Controlled responses; Emotion regulation; Ostracism; Rejection; Social brain; Social exclusion; Social pain;
Social Brain, Social exclusion, Rejection, Ostracism, Social Pain, Automatic Responses, Controlled Responses, Emotion Regulation, Affiliative Responses, Aggressive Responses
English
Social exclusion: Psychological approaches to understanding and reducing its impact
Riva, P; Eck, J
2016
9783319330310
Springer International Publishing
251
273
Chester, D., Riva, P. (2016). Brain mechanisms to regulate negative reactions to social exclusion. In P. Riva, J. Eck (a cura di), Social exclusion: Psychological approaches to understanding and reducing its impact (pp. 251-273). New York, NY : Springer International Publishing [10.1007/978-3-319-33033-4_12].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/122250
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