Stress Reactivity and Corticolimbic Response to Emotional Faces in Adolescents

Abstract

Objective Adolescence is a critical period in the development of lifelong patterns of responding to stress. Understanding underpinnings of variations in stress-reactivity in adolescents is important, as adolescents with altered stress-reactivity are vulnerable to negative risk-taking behaviors including substance use, and have increased lifelong risk for psychopathology. While both endocrinological and corticolimbic neural system mechanisms are implicated in the development of stress-reactivity patterns, the roles of these systems and interactions between the systems in reactivity to social stimuli in adolescents are not clear. We investigated the relationship between cortisol response to a lab-based social stressor and regional brain responses to emotional face stimuli in adolescents. Method Changes in cortisol levels following the Trier Social Stress Test-Child version (TSST-C) were measured in twenty-three disadvantaged and chronically stressed adolescents who also participated in functional magnetic resonance imaging during processing of emotional faces and structural magnetic resonance imaging. The relationships between changes in cortisol following the TSST-C with regional brain activation during face processing, as well as with regional brain morphology, were assessed. Results Cortisol change on the TSST-C showed a significant inverse relationship with left hippocampus to fearful faces (p<0.05, corrected); significant associations to volume were not observed. Conclusions Increased cortisol response to the Trier social stressor was associated with diminished response of the left hippocampus to faces depicting fear. This suggests HPA-corticolimbic system mechanisms may underlie vulnerability to maladaptive responses to stress in adolescents that may contribute to development of stress-related disorders.

Stress Response to the Functional Magnetic Resonance Imaging Environment in Healthy Adults Relates to the Degree of Limbic Reactivity during Emotion Processing

“…major depressive disorder and anxiety disorders). Alternatively, these patterns in healthy subjects may result in increased heterogeneity in control samples that weakens control and patient comparisons [11,12,13]. …”

“…Experimental and neuroimaging research on the neural correlates of cortisol has largely focused on the hippocampus, amygdala, and the prefrontal cortex (PFC) [5,9]. Following stress, increased activity in the hippocampus facilitates downregulation of the HPA axis via inhibitory connections to the paraventricular nucleus of the hypothalamus [10], revealing an inverse relationship between hippocampal activation and the cortisol response to stress [11,12,13]. Conversely, increased activation in the amygdala is correlated with increased cortisol levels, suggesting that the amygdala is involved in the recruitment and ongoing excitation of the HPA axis [14,15].…”

Biological Contributions to Addictions in Adolescents and Adults: Prevention, Treatment, and Policy Implications

“…Environmental factors related to differences in acculturation, cultural expectations, socioeconomics, stress exposure and other domains also warrant consideration as these might differ across cultural groups [137, 140]. Some of these factors (e.g., stress exposure like childhood trauma) have been linked both to the propensity to develop addictions and to brain structure and function, including in regions implicated in reward, motivation and addictions [141, 142], although the precise natures of these relationships warrant further investigation in longitudinal studies in people [143-145]. As such, disentangling the precise contributions to addictions amongst different racial/ethnic groups is both an important and complex undertaking.…”

“…For example, early life adversity has been linked to altered brain structure and function [141, 142]. Additionally, individuals lower in social status show hypo-functioning striatal systems, and this may influence reward- and motivation-related behaviors including addiction propensity [205].…”

Acute cortisol reactivity attenuates engagement of fronto-parietal and striatal regions during emotion processing in negative mood disorders

“…Following fearful eliciting stimuli, increased activity in the hippocampus is understood to facilitate down-regulation of the HPA axis via inhibitory connections to the paraventricular nucleus of the hypothalamus (Jankord and Herman, 2008), resulting in an inverse association between hippocampal activation and cortisol secretion (Kern et al, 2008; Liu et al, 2012; Pruessner et al, 2008). Increased activation in both the amygdala and insula has been positively related to cortisol levels, suggesting that these regions, which underlie saliency, emotion, and attention, also participate in the recruitment and ongoing stimulation of the HPA axis (Langenecker et al, 2012).…”