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Studies using transcranial magnetic stimulation with simultaneous electroencephalography (TMS-EEG) revealed an imbalance between cortical excitation and inhibition (E/I) in the dorsolateral prefrontal cortex (DLPFC) in depression. As adolescence is a developmental period with an increase in depression prevalence and profound neural changes, it is crucial to study the relationship between depression and cortical excitability in adolescence. We aimed to investigate the cortical excitability of the DLPFC in adolescents with depression and a dependency of the TMS-evoked potential N100 on the depression severity. 36 clinical patients (12–18 years of age; 21 females) with a major depressive episode were assessed twice in a longitudinal design: shortly after admission (T0) and after six weeks of intervention (T1). GABA-B-mediated cortical inhibition in the left and right DLPFC, as assessed by the N100, was recorded with EEG. Significantly higher depression scores were reported at T0 compared to T1 (p < 0.001). N100 amplitudes were significantly increased (i.e., more negative) at T0 compared to T1 (p = 0.03). No significant hemispheric difference was found in the N100 component. The correlation between the difference in depression severity and the difference in N100 amplitudes (T0–T1) obtained during stimulation of the left DLPFC did not remain significant after correction for testing in both hemispheres. Higher N100 amplitudes during a state of greater depression severity are suggestive of an E/I imbalance in the DLPFC in adolescents with an acute depressive episode. The N100 reduction potentially reflects a normalization of DLPFC over inhibition in association with decreased depressive symptomatology, indicating severity dependency.
Objective: The current study explored the role of maternal depressive symptoms in the intergenerational transmission of childhood maltreatment and developmental psychopathology. Based on the sensitive window hypothesis, the effects of earlier versus later maternal depression symptoms on child development were analysed.
Method: Ninety-nine mother-child dyads, 65% of which had high-risk teenage mothers, participated in a longitudinal study with three assessments in the first 18 months of the child’s life (T1–T3) and a 4th reassessment (T4) at the child’s preschool age. Using serial mediation analyses, we tested whether the relationship between the mother’s own maltreatment history (Childhood Experience of Care and Abuse Questionnaire) and the child’s psychopathological outcome at preschool age was mediated in a causal effect chain by maternal depression in the first 2 years of life, by current maternal depression (Beck Depression Inventory-II) and by current maternal child abuse potential (Child Abuse Potential Inventory). The children’s emotional problems and externalizing symptoms were assessed at preschool age by parent or teacher Strengths and Difficulties Questionnaire ratings.
Results: The results indicated that especially later maternal depression mediated the relationship between maternal childhood maltreatment and negative developmental outcomes in the next generation. The effects of maltreatment type on maternal depression were rather nonspecific. However, mental abuse affected existing risk factors more directly over time compared to physical and sexual abuse. Additionally, the impact of early life maltreatment and maternal depression on child psychopathology varied by rater. The pathway to externalizing symptoms was significant only in teacher ratings and for the pathway to emotional problems only in maternal ratings.
Conclusions: The present findings suggest that early maternal depression followed by ongoing maternal depression plays a mediating role in the intergenerational cycle of maltreatment. Therefore, in the future, interventions should be offered at an early stage, but also extend well beyond the first 2 years of a child’s life, addressing maternal depression and trauma.