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

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.

Blocking the Mineralocorticoid Receptor in Humans Prevents the Stress-Induced Enhancement of Centromedial Amygdala Connectivity with the Dorsal Striatum

“…Furthermore, the emotional face-matching task does not contain a direct explicit memory component. Although we did find that stress increased task-related activity in the insula, we did not observe an increase in salience network activity in general, which is in contrast to earlier reports (eg, Hermans et al, 2011). This might be explained by differences in the design (movie watching vs specific task) and differences in delay between stress induction and data acquisition (during the first 2 min of stress induction as opposed to during a task starting 10 min after stress induction onset).…”

“…Activation of the NE-LC system together with the peripheral sympatho-adrenomedullary system leads to the rapid release of catecholamines, exciting the salience network in humans (Hermans et al, 2011) and enhancing vigilance. Activation of the HPA axis, conversely, results in a somewhat slower action of corticosteroids, which bind to two receptors in the brain, the glucocorticoid receptor (GR) and the MR.…”

“…Encountering acute threat appears to shift neural network balance (Hermans et al, 2011). This reallocation of neural resources alters cognition and behavior, preferring sensory processing and fast responding over elaborate, flexible behavior.…”

“…According to their respective focus on either the fast-acting NE or the somewhat slow-acting cortisol, researchers also used different stress-induction procedures to either increase arousal and NE levels (eg, violent movies; Hermans et al, 2011) or cortisol levels (eg, social evaluation or cold pressure tasks; Schwabe et al, 2007). Moreover, these lines of research investigated stress-effects in different time domains.…”

Heightened emotional contagion in mild cognitive impairment and Alzheimer’s disease is associated with temporal lobe degeneration

“…The salience network, with hubs in pregenual anterior cingulate cortex and frontoinsula and connections to emotion generators including the amygdala, hypothalamus, and brainstem (26), is hypothesized to be essential for survival-relevant affective stimuli detection and visceromotor emotion generation (29). Heightened salience network connectivity in healthy individuals has been associated with negative emotional reactivity and glucocorticoid levels (e.g., cortisol), a neuroendocrine index of the stress response (30). In AD, increased salience network connectivity relates to neuropsychiatric hyperactivity symptoms (e.g., agitation, irritability, aberrant motor behavior, disinhibition, and euphoria) (31).…”