Journal of affective disorders · 2026
Acute stress alters prefrontal resting-state networks and tES restores functional connectivity.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Guo Zhihua, Gong Yue, Qiu Rui, Yang Liu, Li Yushan, Lu Hongliang, Zhu Xia
Аннотация
BACKGROUND: Acute stress is known to alter resting-state brain connectivity. However, the specific effects on prefrontal networks and whether they can be proactively mitigated remain unclear. This study investigated these stress-induced changes in prefrontal connectivity and evaluated whether pre-stress transcranial electrical stimulation (tES) could offset these effects.
METHODS: In Experiment 1, 86 healthy male undergraduates (mean age = 20.28 ± 1.56 years) were randomly assigned to stress or control groups. In experiment 2, 110 male undergraduates (mean age = 20.86 ± 1.73 years) were assigned to receive active tDCS, active tACS, or sham stimulation targeting the left dorsolateral prefrontal cortex (DLPFC) before stress. In both experiments, the Trier Social Stress Test for Groups was employed to induce acute stress. Resting-state functional near-infrared spectroscopy (fNIRS) was performed before and after intervention.
RESULTS: Acute stress suppressed adaptive interhemispheric connectivity, enhanced connectivity involving the frontal eye field (FEF), and reduced the degree centrality and nodal efficiency of the left DLPFC. The application of either active tDCS or tACS prior to stress counteracted these alterations, reducing overall prefrontal-wide and FEF-related connectivity. Notably, tACS reduced connectivity in a greater number of channel pairs and showed more widespread effects across the prefrontal cortex compared with tDCS, although direct statistical comparisons between the two active stimulation modalities did not consistently reach significance.
CONCLUSIONS: Acute stress altered prefrontal connectivity and centrality, whereas pre-stress tES counteracted these changes. These results highlight tES, particularly tACS, as a promising protective intervention for acute stress-induced disruption of brain connectivity. These findings advance the understanding of stress-related prefrontal network dysfunction and support the potential of neuromodulation for stress management and related clinical applications.
METHODS: In Experiment 1, 86 healthy male undergraduates (mean age = 20.28 ± 1.56 years) were randomly assigned to stress or control groups. In experiment 2, 110 male undergraduates (mean age = 20.86 ± 1.73 years) were assigned to receive active tDCS, active tACS, or sham stimulation targeting the left dorsolateral prefrontal cortex (DLPFC) before stress. In both experiments, the Trier Social Stress Test for Groups was employed to induce acute stress. Resting-state functional near-infrared spectroscopy (fNIRS) was performed before and after intervention.
RESULTS: Acute stress suppressed adaptive interhemispheric connectivity, enhanced connectivity involving the frontal eye field (FEF), and reduced the degree centrality and nodal efficiency of the left DLPFC. The application of either active tDCS or tACS prior to stress counteracted these alterations, reducing overall prefrontal-wide and FEF-related connectivity. Notably, tACS reduced connectivity in a greater number of channel pairs and showed more widespread effects across the prefrontal cortex compared with tDCS, although direct statistical comparisons between the two active stimulation modalities did not consistently reach significance.
CONCLUSIONS: Acute stress altered prefrontal connectivity and centrality, whereas pre-stress tES counteracted these changes. These results highlight tES, particularly tACS, as a promising protective intervention for acute stress-induced disruption of brain connectivity. These findings advance the understanding of stress-related prefrontal network dysfunction and support the potential of neuromodulation for stress management and related clinical applications.