Emotional intelligence mediates the protective role of the orbitofrontal cortex spontaneous activity measured by fALFF against depressive and anxious symptoms in late adolescence

As a stable personality construct, trait emotional intelligence (TEI) refers to a battery of perceived emotion-related skills that make individuals behave effectively to adapt to the environment and maintain well-being. Abundant evidence has consistently shown that TEI is important for the outcomes of many mental health issues, particularly depression and anxiety. However, the neural substrates involved in TEI and the underlying neurobehavioral mechanism of how TEI reduces depression and anxiety symptoms remain largely unknown. Herein, resting-state functional magnetic resonance imaging and a group of behavioral measures were applied to examine these questions among a large sample comprising 231 general adolescent students aged 16-20 years (52% female). Whole-brain correlation analysis and prediction analysis demonstrated that TEI was negatively linked with spontaneous activity (measured with the fractional amplitude of low-frequency fluctuations) in the bilateral medial orbitofrontal cortex (OFC), a critical site implicated in emotion-related processes. Furthermore, structural equation modeling analysis found that TEI mediated the link of OFC spontaneous activity to depressive and anxious symptoms. Collectively, the current findings present new evidence for the neurofunctional bases of TEI and suggest a potential brain-personality-symptom pathway for alleviating depressive and anxious symptoms among students in late adolescence.

Automated summary

Trait emotional intelligence (TEI) is an important personality trait that influences mental health outcomes. This study used neuroimaging and behavioral measures to reveal a negative correlation between TEI and spontaneous activity in the bilateral medial orbitofrontal cortex (OFC), a region associated with emotion processing. The findings suggest that TEI may mitigate depressive and anxious symptoms by modulating activity in the OFC.