Neural sensitivity to peer feedback and the development of social anxiety in adolescent girls

• In Event: Neural response to social feedback from parents and peers: Links to adolescent emotional health

Abstract

Social anxiety (SA) in girls often emerges during adolescence, a time when the brain is highly attuned to social feedback from peers. Evidence suggests that altered sensitivity to threat (i.e. rejection) and reward (i.e. praise) from peers may play a role in the development of social anxiety, but prospective longitudinal data are needed using peer-relevant stimuli. We tested a model proposing that neural sensitivity to threat from peers in early adolescence is associated with decreases in responsivity to reward from peers in mid-adolescence, which in turn accounts for increases in SA.

Participants were 129 adolescent girls (ages 11-13 at T1, M=12.3 years), with approximately 2/3 of the sample at high risk for social anxiety due to shy/fearful temperament. At baseline (T1) and two-year follow-up (T2), diagnosticians assessed SA symptoms and girls completed the Chatroom Interact task (CHAT) and Peer Social Incentive Delay (P-SID) Task to measure neural responses to social reward (positive feedback) and threat (rejection feedback) from fictitious peers that the girls believed they were interacting with. We extracted parameter estimates of neural activity in anatomically-defined regions-of-interest (ROIs) during social threat (vs. baseline) on the CHAT Task (subgenual anterior cingulate cortex [sgACC], dorsal anterior cingulate cortex [dACC], anterior insula [AI], and amygdala) and during social reward (vs. baseline) on the P-SID task (nucleus accumbens [NAcc], putamen, caudate, and medial prefrontal cortex [mPFC]). In separate models, we tested how neural activity in social threat ROI’s to rejection (Chatroom) at T1 predicted activity in the reward ROI’s (P-SID) to positive feedback at T2 (controlling for T1 threat response). We also examined T2 neural activity to social reward as a mediator of the association between T1 neural activity to social threat and T2 SA symptoms, controlling for T1 SA symptoms and neural activity to positive social feedback.

Contrary to hypotheses, we found that girls with higher sgACC activation to rejection (vs. baseline) at T1 showed higher caudate and AI responsivity to positive social feedback (vs. baseline) at T2. As depicted in Figure 1, T2 caudate activation to positive social feedback mediated the association between sgACC activation to rejection and SA symptoms. Thus, girls with higher neural reactivity to rejection feedback in early adolescence showed higher neural reactivity to social reward feedback in mid-adolescence, which appears to place them at higher risk for SA.

Sensitivity to negative feedback from peers in the sgACC, an area involved in monitoring and generating emotion in response to social feedback, appears to amplify the reward circuit’s responsivity to positive feedback from peers. The caudate in particular plays a role in reward learning and reward prediction errors; high caudate activation to reward could suggest that these girls were surprised at being socially rewarded. Girls who are more sensitive to social rejection in early adolescence may find social reward in mid adolescence more surprising because they expect to be rejected, laying the groundwork for the development of SA. Findings could also suggest that high neural reactivity to any form of social evaluation is a risk factor for SA.

Authors

• Jennifer S. Silk, University of Pittsburgh
  Presenting Author

• Stefanie Sequeira, University of Pittsburgh

• Neil P Jones, University of Pittsburgh

• Emily Anne Hutchinson, University of Pittsburgh

• Cecile D Ladouceur, University of Pittsburgh