Search
Browse By Day
Browse By Time
Browse By Panel
Browse By Session Type
Browse By Topic Area
Browse Posters
Search Tips
Register for SRCD23
Personal Schedule
Welcome Letter
Program Guide
Change Preferences / Time Zone
Sign In
Introduction and Hypotheses: Children exposed to childhood adversity (CA) characterized by threat (e.g., physical abuse, sexual abuse, witnessing domestic violence) are particularly prone to exhibiting emotion reactivity deficits (Lambert et al., 2017; Sheridan et al., 2014; Sheridan et al., 2016), in part because threat exposure negatively alters the development of the neuroendocrine systems that underlie emotion reactivity, including the neural circuitry involved in processing environmental stimuli and cortisol production following perceived environmental stressors (Busso et al., 2016; Cicchetti & Rogosch, 2001; Marusak et al., 2015; Thompson et al., 2014). In contrast, deprivation exposure (e.g., neglect, low cognitive stimulation) is hypothesized to increase psychopathology risk in part through its impact on developing neural regions (e.g., dorsolateral prefrontal cortex [dlpfc]) involved in executive functioning, which is also key in emotion processing and modulation. Because neural and physiologic systems work together to facilitate emotion reactivity, assessing how dimensions of CA (i.e., threat, deprivation) impact the association between these systems represents a critical step in the accurate characterization of emotion reactivity following CA. However, most research investigating the impact of CA on components of neurobiological development has been conducted in relatively separate literatures and employed a cumulative approach to measuring CA, barring conclusions on specific pathways between dimensions of CA and emotion reactivity processes.
Methods and Study Population: This study investigates threat and deprivation as potential moderators of the association between (a) neural activity in response to a negative image processing fMRI task and (b) cortisol production following a modified version of the Trier Social Stress Test (TSST). The sample includes 122 adolescent females (M = 12.74 years, SD = 1.92) at elevated risk for internalizing problems. Area under the curve with respect to ground (AUCg) was computed to capture post-TSST cortisol production, self-report measures were used to assess threat and deprivation, and differences in BOLD response during contrasts of negative > neutral images were used as an index of neural reactivity to negative stimuli.
Results: Whole-brain analyses examining neural reactivity as a function of AUCg revealed that AUCg was associated with increased activity in the bilateral temporal pole, bilateral orbital frontal regions, anterior insula, and hippocampus. In analyses testing CA as a moderator of the association between cortisol and select neural regions of interest, amygdala activation interacted with threat exposure to predict AUCg (b = -3.67, p = .009) and dlPFC activation interacted with deprivation exposure to predict AUCg (b = 5.77, p = .040). Findings contribute to a growing field of research connecting physiological and neural emotional processing and response systems, and suggest that dimensions of CA may uniquely disrupt associations between different neural regions and cortisol production.
Meredith Gruhn, University of North Carolina at Chapel Hill
Presenting Author
Adam Bryant Miller
Matteo Giletta, Ghent University
Paul David Hastings, University of California - Davis
Matthew K. Nock, Harvard University
Karen Rudolph, University of Illinois at Urbana-Champaign
George M Slavich, University of California, Los Angeles
Mitchell J Prinstein, University of North Carolina at Chapel Hill
Margaret A. Sheridan, University of North Carolina at Chapel Hill