Page 248 - Like me, or else... - Michelle Achterberg

Chapter 9
explained by genetic and environmental factors. Some children might be more sensitive to social evaluation due to genetic predisposition, but likewise, children might be more prone to retaliation due to environmental influences such as violent video games (Konijn et al., 2007). Unraveling these contributions is important as little is known about the genetic and environmental influences on brain responses to social feedback and regulatory responses. Behavioral genetic modeling can estimate the proportion of variance that is explained by additive genetics (A), common environment (C) and unique environment and measurement error (E).
In chapter 4, I used behavioral genetic modeling to investigate the heritability of social feedback processing and subsequent aggression in middle childhood (ages 7-9-years). Behavioral genetic modeling revealed that aggression following negative feedback was influenced by genetic as well as shared and unique environmental influences. Experimental neuroimaging analyses of a large childhood sample (N=512) showed again that the AI and ACCg responded to both positive and negative feedback (see also chapter 2 and 3), showing this social salience network is already present in childhood. Similar to what was observed in the pilot-test-replication study (chapter 2); positive feedback resulted in increased activation in caudate, supplementary motor cortex (SMA), as well as in the DLPFC. In this study I further observed that the MPFC and inferior frontal gyrus (IFG) were more strongly activated after negative feedback. To test relations with behavior in more detail, post-hoc analyses were performed using the significant whole brain clusters as ROIs. These analyses demonstrated that decreased SMA and DLPFC activation after negative feedback (relative to positive) was associated with more aggressive behavior after negative feedback. Thus, similar to what was observed in adults in chapter 3, in children the DLPFC was an important region for aggression regulation. Moreover, genetic modeling showed that 13%–14% of the variance in DLPFC activity was explained by genetics. These results suggest that the processing of social feedback is partly explained by genetic factors. Moreover, whereas the social salience network seemed to be in place already in middle childhood, the aggression regulation mechanism was less pronounced in middle childhood than in adults, which might suggest that this network is still developing during childhood. A final intriguing finding in chapter 4 was that the behavioral response to aggression (i.e., noise blast) was influenced by shared environment factors. Together, these findings set the stage to examine how brain responses (influenced by genetic factors) and behavior (influenced by shared environment factors) change over time.
Chapter 5 set out to test exactly this question, that is, to test developmental changes in aggression regulation and the underlying neural mechanisms using a longitudinal design. In this chapter I examined how changes in neural activity across childhood were related to change in behavioral development. For this purpose 492 same-sex twins (246 families of the original 256 families) underwent two fMRI sessions across the transition from middle
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