Development of neural systems for processing social exclusion from childhood to adolescence

Bolling, Danielle; Pitskel, Naomi B.; Deen, Ben; Crowley, Michael J.; Mayes, Linda C.; Pelphrey, Kevin A.

doi:10.1111/j.1467-7687.2011.01087.x

Cited by 94 publications

(111 citation statements)

References 71 publications

(116 reference statements)

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“…Since sACC contribution was only observed in a single patient implanted in this region, this result should be taken cautiously. Nevertheless, one may note that our observation is consistent with the known role of sACC in pain processing (Somerville et al 2006;Bolling et al 2011a, b;Sebastian et al 2011). …”

Section: Discussionsupporting

confidence: 77%

“…(Somerville et al 2006). Within this context, it can be argued that it is the sACC that is linked to the pure feeling of social pain (Somerville et al 2006;Bolling et al, 2011a, b;Sebastian et al 2011). In agreement with this claim, sACC activity has been shown to be greater in adolescents experiencing distress after peer rejection (Masten et al 2009) and reduced when people are experiencing exclusion in the presence of social emotional support (Onoda et al 2009).…”

Section: Discussionmentioning

confidence: 99%

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Theta Signal as the Neural Signature of Social Exclusion

et al. 2012

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The feeling of being excluded from a social interaction triggers social pain, a sensation as intense as actual physical pain. Little is known about the neurophysiological underpinnings of social pain. We addressed this issue using intracranial electroencephalography in 15 patients performing a ball game where inclusion and exclusion blocks were alternated. Time-frequency analyses showed an increase in power of theta-band oscillations during exclusion in the anterior insula (AI) and posterior insula, the subgenual anterior cingulate cortex (sACC), and the fusiform "face area" (FFA). Interestingly, the AI showed an initial fast response to exclusion but the signal rapidly faded out. Activity in the sACC gradually increased and remained significant thereafter. This suggests that the AI may signal social pain by detecting emotional distress caused by the exclusion, whereas the sACC may be linked to the learning aspects of social pain. Theta activity in the FFA was time-locked to the observation of a player poised to exclude the participant, suggesting that the FFA encodes the social value of faces. Taken together, our findings suggest that theta activity represents the neural signature of social pain. The time course of this signal varies across regions important for processing emotional features linked to social information.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Theta Signal as the Neural Signature of Social Exclusion

et al. 2012

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“…Social stimuli are especially salient if they are self-relevant, and previous studies either have used stimuli such as images, videos, or audio clips of loved ones (e.g., Hooley et al, 2005; Leibenluft et al, 2004; Whittle et al, 2012) or have employed paradigms that mimic situations participants encounter in the real world (e.g., playing a computer game with peers, as in Eisenberger et al, 2003). Thus, it is valuable to note that our mPFC results echo findings for adolescents’ response to social evaluation paradigms, such as those reported with the social-exclusion cyberball task (Bolling et al, 2011) and with a simulated chat room task (Silk et al, 2012). It is not surprising that mPFC function is sensitive to social reward in various forms, such as being liked, being included, and being selected for interaction.…”

Section: Discussionsupporting

confidence: 75%

Social anhedonia and medial prefrontal response to mutual liking in late adolescents

Healey

Morgan

Musselman

et al. 2014

Brain and Cognition

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Anhedonia, a cardinal symptom of depression defined as difficulty experiencing pleasure, is also a possible endophenotype and prognostic factor for the development of depression. The onset of depression typically occurs during adolescence, a period in which social status and affiliation are especially salient. The medial prefrontal cortex (mPFC), a region implicated in reward, self-relevant processing, and social cognition, exhibits altered function in adults with anhedonia, but its association with adolescent anhedonia has yet to be investigated. We examined neural response to social reward in 27 late adolescents, 18–21 years old, who varied in social anhedonia. Participants reported their social anhedonia, completed ratings of photos of unfamiliar peers, and underwent a functional magnetic resonance imaging task involving feedback about being liked. Adolescents with higher social anhedonia exhibited greater mPFC activation in response to mutual liking (i.e., being liked by someone they also liked) relative to received liking (i.e., being liked by someone whom they did not like). This association held after controlling for severity of current depressive symptoms, although depressive severity was also associated with greater mPFC response. Adolescents with higher levels of social anhedonia also had stronger positive connectivity between the nucleus accumbens and the mPFC during mutual versus received liking. These results, the first on the pathophysiology of adolescent anhedonia, support altered neural reward-circuit response to social reward in young people with social anhedonia.

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“…20,21 This feeling affects adults, adolescents, and children, [22][23][24] and youths who experience early adversity are at highest risk for being rejected by their peers. 25 Indeed, children who have experienced early adversity are less popular and more frequently rejected by their peers from an early school age through to late adolescence.…”

mentioning

confidence: 98%