Page 249 - Like me, or else... - Michelle Achterberg
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Summary and general discussion
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childhood (7-9 years) to late childhood (9-11 years). Results showed that behavioral aggression after social evaluation decreased over time, and this decrease was most pronounced for aggression after positive and neutral social feedback. Confirmatory ROI analyses showed that neural activity in the AI, MPFC and DLPFC increased across childhood, whereas activity in the IFG did not show developmental change. Moreover, increased activity in AI was correlated with more aggression, whereas increased activity in DLPFC was correlated with less aggression. Whole brain-behavior analyses confirmed that bilateral DLPFC activity was correlated with less subsequent aggression following negative social feedback. Finally, longitudinal comparisons revealed that a larger increase in DLPFC activity across childhood was related to a larger decrease in behavioral aggression after negative social feedback over time. These results provide insights on how the developing brain processes social feedback and suggest that the DLPFC serves as an emotion regulation mechanism when dealing with negative social feedback. The results provide a window for understanding individual differences in these developmental trajectories, showing that some children develop stronger regulation skills already in childhood.
Functional architecture of the childhood brain
Previous neurodevelopmental studies and theoretical frameworks have suggested that social emotion regulation might rely on a network of integrated connections between limbic/subcortical and cortical brain regions (Casey, 2015). Most prior studies focused on adolescence or included small samples of children and therefore little is known about functional brain connectivity in childhood. To overcome this gap in knowledge, in chapter 6 I investigated the robustness of findings regarding subcortical-PFC functional brain connectivity in childhood, and the heritability of these connections in 7-to-9-year-old twins. I specifically focused on two key subcortical structures: the ventral striatum (VS) and the amygdala. Reassuringly, I observed strongly replicable brain connectivity patterns over two genetically independent samples of 7- to-9-year-old children, both in the whole brain seed-based analyses and in the post-hoc ROI analyses. Behavioral genetic analyses revealed that VS and amygdala connectivity showed distinct influences of genetics and the environment. VS-PFC connections were best described by genetic and unique environmental factors, whereas amygdala- PFC connectivity was mainly explained by environmental influences (both shared and unique). Similarities were also found: connectivity between the ventral ACC and both subcortical regions showed influences of shared environment, while connectivity with the orbitofrontal cortex (OFC) showed stronger evidence for heritability. Together, this study provides the first evidence for a comprehensive analysis of genetic and environmental effects on subcortical-prefrontal cortex interactions in childhood. The findings demonstrate the need to understand not
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