Stress-Related Noradrenergic Activity Prompts Large-Scale Neural Network Reconfiguration

TLDR

Acute stress shifts the brain into a rapid defense state, likely driven by stress‑related neuromodulators that alter large‑scale neural population properties. The study examined this brain‑state shift in human participants. During a fear‑related acute stressor, responsiveness and interconnectivity within a distributed cortical‑subcortical network rose with stress magnitude, an effect attenuated by β‑adrenergic blockade but not by cortisol synthesis inhibition, indicating that noradrenergic activation drives prolonged coupling between autonomic‑neuroendocrine and attentional‑reorienting regions.

Abstract

Acute stress shifts the brain into a state that fosters rapid defense mechanisms. Stress-related neuromodulators are thought to trigger this change by altering properties of large-scale neural populations throughout the brain. We investigated this brain-state shift in humans. During exposure to a fear-related acute stressor, responsiveness and interconnectivity within a network including cortical (frontoinsular, dorsal anterior cingulate, inferotemporal, and temporoparietal) and subcortical (amygdala, thalamus, hypothalamus, and midbrain) regions increased as a function of stress response magnitudes. β-adrenergic receptor blockade, but not cortisol synthesis inhibition, diminished this increase. Thus, our findings reveal that noradrenergic activation during acute stress results in prolonged coupling within a distributed network that integrates information exchange between regions involved in autonomic-neuroendocrine control and vigilant attentional reorienting.