Electrophysiological markers of stress on working memory networks in adolescents
Alana Campbell1,2, Jessica Graham1, Margaret Nicopolis1,2, Louis Murphy1, Hannah Waltz1, Ashley Williams1, Candace Killian-Farrell1,2, Aysenil Belger1,2; 1University of North Carolina at Chapel Hill, 2Carolina Institute for Developmental Disabilities
Risk for many psychological diseases have an onset in late adolescence and may be initiated or exacerbated by stress. This window of adolescence is marked by cortical growth and neural network development. Stress mediates plasticity of this development, modulates working memory, and plays a role in the etiology of psychological diseases, including psychosis. In this study, we tested the differential impact that stress may have on working memory in adolescents with (high, n = 33) or without (low, n = 35) familial risk for psychiatric disease. We recorded their brainwaves during an n-back task (with n = 0,1,2) before and after the Trier Social Stress Test (TSST). The TSST reliably elicits a stress response, measured via hear-rate variability and cortisol. We predicted that adolescents at greater risk would exhibit reduced P3 amplitude and reduced theta (4-8Hz) power with increased load and post stress. We observed that the high risk group has an overall reduced P3 amplitude (p < .001), accompanied by greater, and more diffuse, theta activity with increased load. These results suggest that adolescents with familial risk for psychiatric illness show evidence of altered neural processing even in the absence of symptoms. Additionally, stress may further disrupt working memory in this group by diminishing synchronous firing in neuronal assemblies and by reducing the strength of the signal.
Topic Area: EXECUTIVE PROCESSES: Working memory