Exploring common changes after acute mental stress and acute tryptophan depletion: Resting-state fMRI studies.

Journal Article (Journal Article)

Stress and low serotonin levels are important biological factors in depression and anxiety etiologies. Although studies indicate that low serotonin levels, stress, and other factors may interact in depression/anxiety psychopathology, few studies have investigated the potentially shared neural substrates. We conducted resting-state fMRI scans pre- and post-stress task, and under control and tryptophan depletion condition, to explore the common changes induced by acute mental stress (AMS) and acute tryptophan depletion (ATD). The present study targeted regions within core brain networks - default mode network, salience network, executive control network, and emotion network - reported altered in AMS and ATD, and used regional homogeneity (ReHo) and functional connectivity (FC) analyses to explore their overlapped effects. We additionally examined the relationships among core neural networks - operationalized as an index of resource allocation bias that quantifies the shift from internal to external modes of processing. We found both manipulations induced increased ReHo of the amygdala and decreased ReHo of the posterior cingulate cortex (PCC). The PCC-amygdala FC was negatively correlated with the change of negative affect, whereas the right dorsolateral prefrontal cortex and right anterior insula FC was positively associated with anxiety level. In addition, we found that a greater shift to an external mode was correlated with higher anxiety level under both conditions. Common changes induced by acute mental stress and acute tryptophan depletion confirmed our hypothesis that AMS and ATD induce changes in common neural pathways, which in turn might mark vulnerability to depression and anxiety.

Full Text

Duke Authors

Cited Authors

  • Zhang, X; Huettel, SA; Mullette-Gillman, OA; Guo, H; Wang, L

Published Date

  • June 2019

Published In

Volume / Issue

  • 113 /

Start / End Page

  • 172 - 180

PubMed ID

  • 30959228

Electronic International Standard Serial Number (EISSN)

  • 1879-1379

Digital Object Identifier (DOI)

  • 10.1016/j.jpsychires.2019.03.025


  • eng

Conference Location

  • England