Dataset Information

The brain's hemodynamic response function rapidly changes under acute psychosocial stress in association with genetic and endocrine stress response markers.

ABSTRACT: Ample evidence links dysregulation of the stress response to the risk for psychiatric disorders. However, we lack an integrated understanding of mechanisms that are adaptive during the acute stress response but potentially pathogenic when dysregulated. One mechanistic link emerging from rodent studies is the interaction between stress effectors and neurovascular coupling, a process that adjusts cerebral blood flow according to local metabolic demands. Here, using task-related fMRI, we show that acute psychosocial stress rapidly impacts the peak latency of the hemodynamic response function (HRF-PL) in temporal, insular, and prefrontal regions in two independent cohorts of healthy humans. These latency effects occurred in the absence of amplitude effects and were moderated by regulatory genetic variants of KCNJ2, a known mediator of the effect of stress on vascular responsivity. Further, hippocampal HRF-PL correlated with both cortisol response and genetic variants that influence the transcriptional response to stress hormones and are associated with risk for major depression. We conclude that acute stress modulates hemodynamic response properties as part of the physiological stress response and suggest that HRF indices could serve as endophenotype of stress-related disorders.

SUBMITTER: Elbau IG

PROVIDER: S-EPMC6205450 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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The brain's hemodynamic response function rapidly changes under acute psychosocial stress in association with genetic and endocrine stress response markers.

Elbau Immanuel G IG Brücklmeier Benedikt B Uhr Manfred M Arloth Janine J Czamara Darina D Spoormaker Victor I VI Czisch Michael M Stephan Klaas Enno KE Binder Elisabeth B EB Sämann Philipp G PG

Proceedings of the National Academy of Sciences of the United States of America 20180910 43

Ample evidence links dysregulation of the stress response to the risk for psychiatric disorders. However, we lack an integrated understanding of mechanisms that are adaptive during the acute stress response but potentially pathogenic when dysregulated. One mechanistic link emerging from rodent studies is the interaction between stress effectors and neurovascular coupling, a process that adjusts cerebral blood flow according to local metabolic demands. Here, using task-related fMRI, we show that ...[more]

PMID: 30201713

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Dataset Information

The brain's hemodynamic response function rapidly changes under acute psychosocial stress in association with genetic and endocrine stress response markers.

Publications

The brain's hemodynamic response function rapidly changes under acute psychosocial stress in association with genetic and endocrine stress response markers.

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