Stress-related noradrenergic activity prompts large-scale neural network reconfiguration
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SourceScience, 334, 6059, (2011), pp. 1151-3
Article / Letter to editor
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PI Group Memory & Emotion
Donders Centre for Cognitive Neuroimaging
PI Group MR Techniques in Brain Function
F.C. Donders Centre for Cognitive Neuroimaging
Subject130 000 Cognitive Neurology & Memory; 130 001 Bridging the gap: hippocampus and memory; 130 026 VENI Hermans, ‘In a fit of fear’; 130 028 Probing the mechanistic underpinnings of stress-related memories; 130 030 The schema-consolidation hypothesis; DCN 1: Perception and Action; DCN 2: Functional Neurogenomics
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. beta-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.
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