Serotonin and emotion regulation: the impact of tryptophan depletion on emotional experience, neural and autonomic activity.

The involvement of serotonin in emotion and psychopathology has been extensively examined. Studies using acute tryptophan depletion (ATD) have found limited effects on mood and aggression, and one of the explanations suggests that serotonin may be involved in higher-order functions, such as emotion regulation. However, there is very limited evidence for this hypothesis. The present study investigated the impact of ATD on emotion regulation in a double-blind, placebo-controlled, crossover design. A sample of psychiatrically healthy men (N = 28) completed a cognitive task assessing reappraisal ability (i.e., the success of using reappraisal, an emotion regulation strategy, to modulate emotional responses), following ATD and placebo. EEG frontal activity and asymmetry, as well as heart-rate variability (HRV), also were assessed in the reappraisal task. Both frequentist and Bayesian methods were employed for statistical analysis. Results indicated that ATD reduced plasma tryptophan, and reappraisal was effective in modulating emotional experience in the emotion regulation task. However, ATD had no significant effect on reappraisal ability, frontal activity, and HRV. These results offer direct and compelling evidence that decreasing serotonin synthesis through ATD does not alter an emotion regulation ability that is considered crucial in mood and aggression and has been linked with transdiagnostic risk of psychopathology.

Resting-state frontal, frontlateral, and parietal alpha asymmetry:A pilot study examining relations with depressive disorder type and severity.

Introduction: The search for biomarkers has been central to efforts of improving clinical diagnosis and prognosis in psychopathology in the last decades. The main approach has been to validate biomarkers that could accurately discriminate between clinical diagnoses of very prevalent forms of psychopathology. One of the most popular electrophysiological markers proposed for discrimination in depressive disorders is the electroencephalography (EEG)-derived frontal alpha asymmetry. However, the validity, reliability and predictive value of this biomarker have been questioned in recent years, mainly due to conceptual and methodological heterogeneity. Methods: In the current non-experimental, correlational study we investigated relationship of resting-state EEG alpha asymmetry from multiple sites (frontal, frontolateral, and parietal) with different forms of depressive disorders (varying in type or severity), in a clinical sample. Results: Results showed that alpha asymmetry in the parietal (P3-P4) was significantly higher than in the frontal (F3-F4) and frontolateral sites (F7-F8). However, we did not find significant relations between alpha asymmetry indices and our depressive disorder measures, except for a moderate positive association between frontolateral alpha asymmetry (eyes-closed only) and depressive disorder severity (determined through clinical structured interview). We also found no significant differences in alpha asymmetry between participants, depending on their depression type. Discussion: Based on results, we propose the parietal and frontolateral asymmetry indices to form hypotheses that should not be abandoned in the depression markers research, but worth for further experimental research. Methodological and clinical implications of the current findings are discussed.