Trajectories of reward and loss neural circuitry across adolescence : examining the effects of early life stress on neurodevelopment
Keywords: Psychology.

Although there is a burgeoning functional magnetic resonance imaging (fMRI) literature, few researchers have conducted longitudinal examinations of neural activation across adolescence. While cross-sectional studies have provided important insights, this approach does not inform us about the development of neural circuitry. Indeed, cross-sectional examinations of reward circuitry and symptomatology do not assess the dynamic nature of either psychopathology or neural activation; thus, these studies overlook critical developmental courses and limit our knowledge in this area. The more comprehensively we examine the interplay between functional patterns of neural activation and behavior, the more information we will have regarding adolescent development, and the more informed will be our efforts to reduce harmful outcomes and improve treatment strategies. In my dissertation, I leverage three timepoints of longitudinal data spanning adolescence to assess typical development and examine how early life stress (ELS) might disrupt certain processes. Indeed, ELS is a risk factor for both psychopathology and aberrant neural reward processing. In Chapter I, I outline the extant literature examining reward, risk, internalizing, and externalizing symptoms. I discuss the importance of conducting longitudinal fMRI research in understanding intra-individual variation in these constructs. Next, I discuss the role of ELS in contributing to reward and loss processing in addition to symptoms of psychopathology. Based on findings from cross-sectional assessments, researchers have posited that NAcc activation is decreased following ELS; we know little, however, about alterations in the trajectories of reward circuitry following adversity and of patterns of neural activation in children as young as 9 years old. 225 participants were richly characterized with respect to their behavioral functioning and neural activation over the course of four years. At each of three timepoints, participants completed an interview assessing ELS, reported on their reward and punishment sensitivity and on their symptoms of internalizing and externalizing symptoms, and underwent fMRI. We measured activation in the NAcc during the anticipation and receipt of gain, and activation in the AIns during the anticipation and receipt of loss across adolescent development and as a function of having experienced ELS. In addition, we utilized these patterns of neural activation to gain a better understanding of the development of symptoms. For the first aim, we sought to characterize typical adolescent behavioral and neural development. We found that: i) trajectories of reward and punishment show age-related increases across adolescence; ii) trajectories of reward and punishment track with trajectories of internalizing and externalizing symptoms; iii) trajectories of NAcc and AIns activation decreased across adolescence; and iv) baseline activation in the NAcc and AIns during the receipt of gain and loss, respectively, predicted changes in externalizing symptoms four years later. For the second aim, we sought to understand how ELS may alter development. We found that: i) participants who experienced more severe ELS had decreasing activation in the NAcc during the receipt of gain across adolescence, whereas participants who experienced less severe ELS remained stable across time; and ii) change in NAcc activation during the receipt of gain mediated the association between ELS and externalizing symptoms in adolescence. Finally, in Chapter III, I summarize the importance of the findings presented in my dissertation, discuss limitations of the current study, expand on strengths of our longitudinal study design, and offer future directions for the field