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An adaptive neural stress response is essential to adequately cope with a changing environment. It was previously argued that sympathetic/noradrenergic activity during acute stress increases salience network (SN) connectivity and reduces executive control network (ECN) connectivity in healthy controls, with opposing effects in the late aftermath of stress. Altered temporal dynamics of these networks in response to stress are thought to play a role in the development of psychopathology in vulnerable individuals.
We exposed male healthy controls (n = 40, mean age = 33.9) and unaffected siblings of schizophrenia patients (n = 39, mean age = 33.2) to the stress or control condition of the trier social stress test and subsequently investigated resting state functional connectivity of the SN and ECN directly after and 1.5 h after stress.
Acute stress resulted in increased functional connectivity within the SN in healthy controls, but not in siblings (group × stress interaction pfwe < 0.05). In the late aftermath of stress, stress reduced functional connectivity within the SN in both groups. Moreover, we found increased functional connectivity between the ECN and the cerebellum in the aftermath of stress in both healthy controls and siblings of schizophrenia patients.
The results show profound differences between siblings of schizophrenia patients and controls during acute stress. Siblings lacked the upregulation of neural resources necessary to quickly and adequately cope with a stressor. This points to a reduced dynamic range in the sympathetic response, and may constitute a vulnerability factor for the development of psychopathology in this at-risk group.
Mather and colleagues postulate that norepinephrine promotes selective processing of emotionally salient information through local “hotspots” where norepinephrine release interacts with glutamatergic activity. However, findings in rodents and humans indicate that norepinephrine is ineffective in modulating mnemonic processes in the absence of a functional amygdala. We therefore argue that emphasis should shift toward modulatory effects of amygdala-driven changes at the network level.
In their target article, Kalisch and colleagues advocate a paradigm shift in research on stress-related mental disorders away from vulnerability factors and toward determinants of resilience. We endorse this shift but argue that their focus on “appraisal style” as the ultimate path to resilience may be too narrow. We illustrate this point by examining recent literature on the role of corticosteroids in resilience.
Mazur & Booth's (1998) target article concerns basal and reciprocal relations between testosterone and dominance, and has its roots in Mazur's (1985; 1994) model of primate dominance-submissiveness interactions. Threats are exchanged in these interactions and a psychological stress-manipulation mechanism is suggested to operate, making sure that face-to-face dominance contests are usually resolved without aggression. In this commentary, a recent line of evidence from human research on the relation between testosterone, cortisol, and vigilant (dominant) and avoidant (submissive) responses to threatening “angry” faces is discussed. Findings, to a certain extent, converge with Mazur & Booth's theorizing. However, the strongest relations have been found in subliminal exposure conditions, suggesting that biological instead of psychological mechanisms are involved.
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