Background
Multiple studies have found a reduced reward positivity (RewP) among individuals with major depressive disorder (MDD). Event-related potential studies have also reported blunted neural responses to pleasant pictures in MDD as reflected by the late positive potential (LPP). These deficits have been interpreted broadly in terms of anhedonia and decreased emotional engagement characteristic of depression.
Methods
In the current study, a community-based sample of 83 participants with current MDD and 45 healthy individuals performed both a guessing task and a picture viewing paradigm with neutral and pleasant pictures to assess the RewP and the LPP, respectively.
Results
We found that both RewP and LPP to pleasant pictures were reduced in the MDD group; moreover, RewP and LPP were both independent predictors of MDD status. Within the MDD group, a smaller RewP predicted impaired mood reactivity in younger but not older participants. Smaller LPP amplitudes were associated with increased anhedonia severity in the MDD group.
Conclusions
These data replicate and merge separate previous lines of research, and suggest that a blunted RewP and LPP reflect independent neural deficits in MDD – which could be used in conjunction to improve the classification of depression.
Individuals with current depression show reduced amplitude of the P300 component of the stimulus‐locked event‐related potential (ERP)—an effect most often examined in oddball tasks. Although imperative stimuli in response‐monitoring paradigms (e.g., the flanker task), also elicit a P300, it is unclear whether a blunted P300 can be observed in depression in these tasks. Moreover, the P300 overlaps with the correct‐response negativity (CRN) and error‐related negativity (ERN), and is similar to the error positivity (Pe)—response‐locked ERPs frequently examined in flanker tasks. The current study examined the stimulus‐locked P300 and response‐monitoring ERPs on error (i.e., ERN, Pe) and correct responses (i.e., CRN) during an arrowhead flanker task in 72 individuals with a current depressive disorder and 42 never depressed healthy individuals. Consistent with findings from oddball tasks, P300 amplitude was reduced among participants with depression. Further, results indicated increased ERN and CRN, and decreased Pe, in depression. However, when the blunted P300 was included in analyses, group differences in response‐monitoring ERPs were no longer evident. Accordingly, P300 amplitudes were correlated negatively with the ERN/CRN and positively with Pe in both groups. A blunted P300 in depression can be observed in speeded response tasks, and can produce apparent increases in ERN and CRN due to ERP component overlap. Further, reduced Pe in participants with depression may reflect a reduced P300 to error commission. These data highlight the central role of reduced P300 in clinical depression, and demonstrate that this effect can be observed across both stimulus‐ and response‐locked ERPs in speeded response tasks.
Neurocognitive impairments commonly observed in depressive disorders are thought to be reflected in reduced P300 amplitudes. To date, depression‐related P300 amplitude reduction has mostly been demonstrated cross‐sectionally, while its clinical implication for the course of depression remains largely unclear. Moreover, the relationship between P300 and specific clinical characteristics of depression is uncertain. To shed light on the functional significance of the P300 in depression, we examined whether initial P300 amplitude prospectively predicted changes in depressive symptoms among a community sample of 58 adults (mean age = 38.86 years old, 81% female) with a current depressive disorder. This sample was assessed at two‐time points, separated by approximately nine months (range = 6.6–15.9). At the initial visit, participants completed clinical interviews, self‐report measures, and a flanker task, while EEG was recorded to derive P300 amplitude. At the follow‐up visit, participants again completed the same clinical interviews and self‐report measures. Results indicated that a reduced P300 amplitude at the initial visit was associated with higher total depressive symptoms at follow‐up, even after controlling for initial depressive symptoms. These data indicate the potential clinical utility for the P300 as a neural marker of disease course among adults with a current depressive disorder. Future research may target P300 in interventions to determine whether depression‐related outcomes can be improved.
Recent research suggests that depressive disorders in adults are characterized by reductions in flanker P300 amplitude, and that a reduced flanker P300 may also predict worst depressive trajectories over time. The current study extended this work to adolescence-and to evaluate the specificity of the relationship between flanker P300 to depressive symptoms versus anxiety symptoms, and whether the association between flanker P300 and depressive symptoms was moderated by biological sex. To this end, P300 amplitude, depression, anxiety, and sex were assessed in a large sample of 619 adolescents aged 11 to 14. Participants completed a speeded response flanker task while EEG was recorded, as well as self-reported measures of current depression and anxiety symptoms. Reduced P300 amplitude was related to both heightened depression and anxiety symptoms in zero-order correlations. Regression-based analyses suggest that reduced P300 was uniquely related to depressive symptoms. Furthermore, this negative association between P300 and depression was apparent in female adolescents, but not male adolescents. In sum, the current study suggests that flanker P300 amplitude may potentially serve as a neural marker specific to depression in females during adolescence.
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