| dc.description.abstract | Depression vulnerability has been frequently linked to selective attention biases, but these biases may partly result from an inhibitory deficit for processing depressive information (Joormann, 2004). Reduced inhibition when encountering sad interpersonal information (e.g., faces) could lead to greater associative processing, deeper encoding among related depressive content in memory, increased rumination, and perhaps could promote depressive episodes. Inhibition and selective attention can be examined through behavioral and psychophysiological indicators, including the N200, P300a, and P300b ERP components. The present study examined whether groups traditionally at risk of depression would show inhibitory deficits for depressive facial expressions as compared to a low-risk group. A 2 x 2 design yielded four groups with two levels of current dysphoria status (yes/no) and history of depression (yes/no), enabling comparisons of relative risk. Each participant completed two visual oddball tasks. In the experimental task, participants responded or inhibited a response to infrequently presented sad or happy target faces in the context of frequently presented neutral faces. In the non-affective control task, participants responded only to faces that fit into one of three broad age groupings. Behavioral (e.g., reaction times, response errors), psychophysiological (ERP components), and self-report (e.g., rumination) measures relevant to selective attention and inhibition were analyzed. Between- and within-groups contrasts were conducted to reveal whether at-risk groups exhibit attentional bias and inhibitory deficiency specific to depressive information. Also, the study examined whether different operationalizations of depression risk evince common or distinct mechanisms of vulnerability. Across the full sample, previous depression was associated with greater P3b amplitude for sad target faces than happy target faces, in contrast with the depression naïve group. However in males, only the combination of previous depression and current dysphoria were linked to elevated P3s following sad targets. Evidence for a sad affect inhibition deficit was limited to dysphoric females' increased errors of commission following sad distracter faces. Results suggest that specific operationalizations of risk may be characterized by an attentional bias toward depressive facial affect in the social environment, which could promote additional depressogenic cognition and social behavior. Theoretical ramifications regarding gender and state versus trait vulnerability are also discussed. | |
