Despite evidence documenting activation of the social pain network in response to social rejection and its link to temporary distress, far less is known regarding its role in pervasive emotional difficulties. Moreover, research has not considered the intersection between neural activation to experimentally induced social exclusion and naturally occurring social adversity. This study examined an integrated social pain model of internalizing symptoms, which posits that (i) neural sensitivity in the social pain network is associated with internalizing symptoms, (ii) this linkage is more robust in youth with than without a history of social adversity, and (iii) heightened avoidance motivation serves as one pathway linking neural sensitivity and internalizing symptoms. During a functional magnetic resonance imaging scan, 47 adolescent girls (M age = 15.46 years, SD = .35) with well-characterized histories of peer victimization were exposed to social exclusion. Whole-brain analyses revealed that activation to exclusion in the social pain network was associated with internalizing symptoms. As anticipated, this linkage was stronger in chronically victimized than non-victimized girls and was partially accounted for by avoidance motivation. This research indicates the importance of integrating neural, social and psychological systems of development in efforts to elucidate risk for internalizing symptoms among adolescent girls.

The present study sought to clarify the trajectory (i.e., continuous vs. discontinuous) and expression (i.e., homotypic vs. heterotypic) of anxiety and depressive symptoms across childhood and adolescence. We utilized a state-of-the-science analytic approach to simultaneously test theoretical models that describe the development of internalizing symptoms in youth. In a sample of 636 children (53% female; Mage = 7.04; SDage = 0.35) self-report measures of anxiety and depression were completed annually by youth through their freshman year of high school. For both anxiety and depression, a piecewise growth curve model provided the best fit for the data, with symptoms decreasing until age 12 (the “developmental knot”) and then increasing into early adolescence. The trajectory of anxiety symptoms was best described by a discontinuous homotypic pattern in which childhood anxiety predicted adolescent anxiety. For depression, two distinct pathways were discovered: A discontinuous homotypic pathway in which childhood depression predicted adolescent depression and a discontinuous heterotypic pathway in which childhood anxiety predicted adolescent depression. Analytical, methodological, and clinical implications of these findings are discussed.

Social reticence (SR) manifests as shy, anxiously avoidant behavior in early childhood. With development, overt signs of SR may diminish but could still manifest in neural responses to peers. Measures of SR were obtained across ages 2-to-7 years. At age 11, pre-adolescents previously characterized as high (N=30) or low (N=23) in SR completed a novel fMRI-based peer interaction task that quantifies neural responses to the anticipation and receipt of distinct forms of social evaluation. While anticipating unpredictable compared with predictable feedback, high relative to low childhood SR was associated with greater activity in dorsal anterior cingulate and bilateral insula, brain regions implicated in processing salience and distress. High SR was also associated with negative functional connectivity between insula and ventromedial prefrontal cortex, a region commonly implicated in affect regulation. Finally, among the high SR group, negative evaluation was associated with increased amygdala activity, but only during feedback from unpredictable peers.

Belonging to a social group is one of the most important factors contributing to well-being. The Belonging Regulation model proposes that humans possess a social monitoring system (SMS) that evaluates social inclusion and monitors belonging needs. Here, we used a prospective longitudinal design to examine links between peer victimization experienced across 7 years and social monitoring at the behavioral and neural level in adolescent girls (n = 38, Mage = 15.43 years, SD = .33). Participants completed a social evaluation task during a functional magnetic resonance imaging (fMRI) scan. More severe peer victimization was associated with increased activation to in-group versus out-group peers in the amygdala, ventral striatum, fusiform gyrus, and temporoparietal junction. Moreover, participants who displayed increased activation in these regions reported lower social self esteem and higher levels of internalizing and externalizing symptoms. These results suggest that exposure to peer victimization across the school years is associated with heightened social monitoring at the neural level during adolescence, which has potential adverse implications for girls’ adjustment and well-being.

Adolescence is a period of heightened emotional reactivity, which is reflected in greater activation in emotion-processing regions of the brain in adolescents relative to children and adults. While elevated emotional reactivity and poor emotion regulation are thought to contribute to the rise in rates of internalizing psychopathology, including anxiety, during adolescence, little research has examined factors predicting individual differences in the neural regulation of emotion that can explain why only some adolescents experience anxiety. To address this gap, the present study examined the contribution of childhood negative emotionality (NE) and cognitive control (CC) to neural processing of emotion in adolescence. A sample of 44 girls (M age = 15.5, SD = 0.35) was selected from a longitudinal study that included self, parent, and teacher report of NE and CC between 2nd and 7th grades. Following 9th grade, girls completed an emotion regulation task during a functional magnetic resonance imaging scan. Neural regulation of emotion was indexed by functional connectivity between the amygdala and right ventrolateral prefrontal cortex (rVLPFC) during emotion regulation. Analyses revealed that NE predicted a less mature pattern of amygdala-rVLPFC connectivity while CC predicted a more mature pattern of amygdala-rVLPFC connectivity. Additionally, we found an interaction between NE and CC, such that NE predicted emotion dysregulation at low but not high levels of CC. Neural dysregulation of emotion was associated with anxiety symptoms across the following nine months. These findings identify important individual differences in the development of emotion dysregulation that contribute to risk for anxiety in adolescence.