In addition individuals who experienced CSA

In addition, individuals who experienced CSA and who develop CSA-related Post-Traumatic Stress Disorder (PTSD) are at increased risk to develop subsequent internalizing disorders (Lindert et al., 2014), which makes internalizing disorders and CSA-related PTSD overlapping in symptomatology. This, in combination with the comparable levels of increased amygdala activation in response to emotional faces (Hart and Rubia, 2012; Monk et al., 2008a,b; Roberson-Nay et al., 2006; Thomas et al., 2001), highlights the need to investigate whether similar underlying neurobiological mechanisms are present in these two groups. To our knowledge, there is no research published that directly compared amygdala responsiveness in adolescents with an internalizing disorder and adolescents with CSA-related PTSD. It is possible that there are neurobiological differences between these two groups: although adolescents with internalizing disorders and adolescents with CSA-related PTSD show a large overlap in symptomatology (Lindert et al., 2014) and amygdala responsiveness to emotional faces (Hart and Rubia, 2012; Monk et al., 2008a,b), adolescents with CSA-related PTSD also have distinct characteristics like the experience of sexual abuse and a different attachment profile (van Hoof et al., 2015). While it VX765 manufacturer is challenging to reveal differentiating neurobiological mechanisms between adolescents with internalizing disorders and adolescents with CSA-related PTSD, one way to examine underlying distinct response patterns is by studying habituation effects. In healthy populations, the amygdala is known to habituate over time in response to emotional faces (Breiter et al., 1996; Fischer et al., 2003). The results of studies investigating habituation of amygdala activation in individuals with inhibited states, depression or anxiety are however inconsistent. For example, a study by Hare et al. (2008) showed that adolescents with higher levels of self-reported anxiety symptoms habituated more slowly to observing emotional faces than adolescents with lower levels of self-reported anxiety symptoms. However, this study did not include information about the type of heightened self-reported anxiety and whether the adolescents experienced CSA. Two other studies reported relatively strong habituation effects in response to face processing within the amygdala, one in a sample of adults with a social anxiety disorder (Sladky et al., 2012) and another in a sample of female students scoring high on fear questionnaires (Wendt et al., 2012). Again, no information on CSA was available. To extend the current literature on habituation, CSA-related PTSD and internalizing disorders, tumor suppressor genes is of interest to compare amygdala habituation patterns in adolescents with internalizing disorders and adolescents with CSA-related PTSD. In this study, we examined amygdala habituation in two groups known to show elevated amygdala responsiveness to emotional faces. We included individuals with a DSM-IV diagnosis of a depressive or anxiety disorder (INT group), adolescents with CSA-related PTSD (CSA-related PTSD group), and a matched healthy control group (CNTR group). Participants performed an emotional face-processing task validated in prior work (Monk et al., 2003; van den Bulk et al., 2013; van den Bulk et al., 2014), and we analysed the data for habituation patterns for subgroups of individuals by separating the task in three runs. We aimed to investigate (1) whether the INT and CSA-related PTSD group show a deviant habituation pattern of amygdala activation compared to the CNTR group and (2) whether there are specific differences between the INT and CSA-related PTSD group in habituation patterns. We expected that the CNTR group shows fast habituation of amygdala activation (Breiter et al., 1996), that the INT and CSA-related PTSD group show increased amygdala activation in response to emotional faces (Garrett et al., 2012; McClure et al., 2007; Roberson-Nay et al., 2006) and that the INT group shows sustained activation of the amygdala (Hare et al., 2008). We were particularly interested in whether adolescents with CSA-related PTSD show a similar pattern of amygdala activation as adolescents with an internalizing disorder, or whether their neural patterns were dissociable, suggesting that although there is a large overlap in symptomatology between INT and CSA-related PTSD, a different underlying neurobiological mechanism is present.