How does our brain control response to stress?

Resting-state activity of the hippocampus predicts stress reaction

January 25, 2013

The way how people react to stress can have a significant influence on their mental health: Especially overreactions of the stress hormone axis to repeated challenges can become a problem. With a new method, scientists of the Max Planck Institute of Psychiatry examined the role of the central nervous brain control in the individual stress response. Numerous interdependent neuronal networks within the brain control our individual adaptation to stressful situations. These networks can also be measured in resting-state, i.e., without any noteworthy external strain. In a study on 20 young healthy men, the researchers investigated the predictability of the individual regulatory capacities of the stress hormone system by means of these resting-state network patterns.

People suffering from stress-related diseases - such as depression or anxiety disorders - often show alterations in the hippocampus, a specific brain area important for learning and memory. Due to its central role in the regulation of the organism's hormonal stress response, anatomical and functional changes in the event of sickness are not surprising. Previously, it was unknown how the superior neuronal regulation influences this region and, as a consequence, the stress-related secretion of cortisol.

Therefore, in their study the researchers first of all determined the individual regulatory capacities of the stress hormone system by means of a hormonal stress simulation test. As expected, the stress hormone values of the healthy participants were in the normal range – however, a considerably broad spectrum of cortisol values measured could be observed, indicating individual differences concerning stress response control.

By using functional imaging techniques, altogether 15 functional neuronal networks with anatomically defined nodes in the brain were examined in the test persons. These neuronal activity patterns were linked with the hormonal stress reactivity of the respective test persons. These correlations identified that individual resting-state networks, especially that of the hippocampus, are predictive for the stress response measured later on. Actually, if the spontaneous signal fluctuations of the left hippocampus were better synchronized with a certain area of the right hippocampus, the test persons showed a significantly lower stress hormone secretion. Other limbic areas, e.g., the amygdala, exhibited an inverse correlation between resting-state activity and stress hormone test.

These results gained here in healthy persons show for the first time that a stronger functional connectivity between special brain regions of the limbic system can possibly mitigate the hormonal stress reaction. The authors hope that by further developing this method, the regulatory system of the stress hormone homeostasis can be characterized in more detail in order to develop biomarkers for stress-related disorders.

BM

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