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Threat exposure moderates associations between neural and physiological indices of emotion reactivity in adolescent females

Authors
  • Gruhn, Meredith
  • Miller, Adam Bryant
  • Eisenlohr-Moul, Tory A.
  • Martin, Sophia
  • Clayton, Matthew G.
  • Giletta, Matteo
  • Hastings, Paul D.
  • Nock, Matthew K.
  • Rudolph, Karen D.
  • Slavich, George M.
  • Prinstein, Mitchell J.
  • Sheridan, Margaret A.
Publication Date
Jan 01, 2024
Source
Ghent University Institutional Archive
Keywords
Language
English
License
Unknown
External links

Abstract

Early life adversity (ELA) characterized by threat (e.g., abuse, witnessing violence) impacts neural and physiologic systems involved in emotion reactivity; however, research on how threat exposure impacts the interplay between these systems is limited. This study investigates ELA characterized by threat as a potential moderator of the association between (a) neural activity during a negative image processing fMRI task and (b) cortisol production following a modified Trier Social Stress Test (TSST). The sample is comprised of 117 young adolescent females (Mage = 11.90 years, SD = 1.69) at elevated risk for internalizing problems. Whole-brain analyses revealed a positive association between cortisol production and increased right lateral orbitofrontal cortex activity during the emotion reactivity task. In moderation models, threat exposure interacted with bilateral amygdala activation (b = -3.34, p = 0.021) and bilateral hippocampal activation (b = -4.14, p = 0.047) to predict cortisol response to the TSST. Specifically, participants with low, but not high, levels of threat exposure demonstrated a positive association between cortisol production and neural activity in these regions, while no significant association emerged for participants with high threat exposure. Findings contribute to the growing field of research connecting physiological and neural emotion processing and response systems, suggesting that dimensions of ELA may uniquely disrupt associations between neural activation and cortisol production.

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