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Poster #20 - The Association between Exposure to Stress and the Neural Correlates of Self-Regulation in Early Childhood

Sat, March 23, 2:30 to 3:45pm, Baltimore Convention Center, Floor: Level 1, Exhibit Hall B

Integrative Statement

Research has demonstrated that early experiences with stress and adversity have a disruptive effect on neural development and cognitive functioning. One cognitive process particularly likely to be affected by stress is self-regulation, as the brain regions underlying self-regulation, including the prefrontal cortex, have a protracted period of development. However, little research has investigated the effects of stress on the neural basis of self-regulation in early childhood. The current study examined how exposure to various risk factors affects the development of the neural correlates of self-regulation in a sample of young children.

Participants included 190 children (84 female) who were part of a wider longitudinal study assessing children at 30, 36, and 42 months. Each child completed a Go/NoGo task and a Passive Auditory Oddball task while electroencephalography data were collected. During the Go/NoGo task, children were instructed to press a button when they saw a fish on the screen (Go stimulus; 60 trials), but not to press the button when they saw a shark on the screen (NoGo stimulus; 20 trials). During the Passive Oddball task, the children watched a muted cartoon while high- and low-pitch tones were played. The task included 120 high- and low-frequency tones (84 frequent tones; 36 infrequent tones), and the pitch of the frequent tone was counterbalanced. Event-Related Potentials (ERPs) were time-locked to stimulus presentation.

Sequential temporal-spatial principal components analysis (PCA) was conducted to identify the time frames and electrode regions accounting for the majority of variability in the waveform across each task. For the Go/NoGo task, the PCA component corresponding to the second negative deflection in the waveform across frontocentral electrodes was identified as the N2 component, while for the Passive Oddball task, the PCA component corresponding to the third positive deflection in the waveform across posterior electrodes was identified as the P3 component (see Figure 1). Some participants (n=61) had longitudinal (or repeated measures) ERP data. However, because no significant change was observed in ERPs over time, ERP amplitude and latency values were averaged across the available assessment points for the children who had multiple assessments.

Based on parent and observer reports at 30-months, along with objective measurement of the child’s sleep, three domains of cumulative risk, biological, sociodemographic, and environmental/familial, quantified the child’s exposure to various stressors. These risk domains are described in Table 1. Pearson correlations examined the association between each risk domain and amplitudes and latencies from each ERP task.

Of the three risk domains, only environmental/familial risk showed a significant association with the morphology of the N2 and P3. Increased exposure to environmental/familial risk was associated with larger NoGo N2 amplitudes (r=-.18), longer NoGo N2 latencies (r=.16), and longer infrequent P3 latencies (r=.14). As more negative NoGo N2 amplitudes are associated with poorer regulatory skills, and longer component latencies are thought to be associated with slower cognitive processing, the current findings suggest that children exposed to increased levels of environmental/familial risk factors show a pattern of neural activity associated with poorer regulation and slower cognitive processing.

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