Mild early-life stress exaggerates the impact of acute stress on corticolimbic resting-state functional connectivity
Number of pages
SourceEuropean Journal of Neuroscience, 55, 9-10, (2022), pp. 2122-2141
Article / Letter to editor
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PI Group Affective Neuroscience
SW OZ BSI KLP
Onderzoekcentrum voor Staat en Recht
PI Group Memory & Emotion
European Journal of Neuroscience
Subject130 000 Cognitive Neurology & Memory; 230 Affective Neuroscience; Experimental Psychopathology and Treatment; Radboudumc 13: Stress-related disorders DCMN: Donders Center for Medical Neuroscience
Abundant evidence shows that early-life stress (ELS) predisposes for the development of stress-related psychopathology when exposed to stressors later in life, but the underlying mechanisms remain unclear. To study predisposing effects of mild ELS on stress sensitivity, we examined in a healthy human population the impact of a history of ELS on acute stress-related changes in corticolimbic circuits involved in emotional processing (i.e., amygdala, hippocampus, ventromedial prefrontal cortex; vmPFC). Healthy young male participants (n=120) underwent resting-state functional magnetic resonance imaging (fMRI) in two separate sessions (stress induction versus control). The Childhood Trauma Questionnaire (CTQ) was administered to index self-reported ELS, and stress induction was verified using salivary cortisol, blood pressure, heart rate, and subjective affect. Our findings show that self-reported ELS was negatively associated with baseline cortisol, but not with the acute stress-induced cortisol response. Critically, individuals with more self-reported ELS exhibited an exaggerated reduction of functional connectivity in corticolimbic circuits under acute stress. A mediation analysis showed that the association between ELS and stress-induced changes in amygdala-hippocampal connectivity became stronger when controlling for basal cortisol. Our findings show, in a healthy sample, that the effects of mild ELS on functioning of corticolimbic circuits only become apparent when exposed to an acute stressor, and may be buffered by adaptations in hypothalamic-pituitary-adrenal axis function. Overall, our findings might reveal a potential mechanism whereby even mild ELS might confer vulnerability to exposure to stressors later in adulthood.
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