Dual Mechanisms Of Negative Affective Priming

Objects: The study aims to investigate whether depressed patients and remitted depressed individuals show valence-dependent inhibition impairment and to investigate its neurophysiological correlates, and to study whether impaired inhibition of negative affect is a cognitive vulnerability factor explaining depression.Methods: Allowing dissociation of inhibitory and episodic retrieval processes. Inhibitory processes are elicited under intact stimulus conditions, whereas episodic retrieval is elicited when target stimuli are degraded. Data collected from 18 patients with depression and 16 remitted depressed individuals and 18 normal controls were analyzed in a negative priming affective (NAP) task using event-related potentials (ERPs) .Results: (1) Compared to normal controls, depressed patients showed shorter time in response to negative NP trials, and longer time in response to positive NP trials in NAP task with intact target stimuli. (2) In addition to the overall reduced P2 amplitude for negative trials and the overall reduced late positive component (LPC) amplitude for positive and negative trials in patients, the ERP differences of different conditions for each group were also found. In response to negative NP targets, the central-parietal P2 amplitude was reduced and LPC latency was shorter in patients, whereas the left central P2 amplitude was larger and the LPC latency was delayed in controls. In response to positive NP targets, the parietal P2 amplitude was enhanced and the LPC latency was delayed in both groups. (3) Compared to normal controls, remitted depressed individual showed shorter time in response to self-descriptive negative targets in NP condition, but longer time for positive targets. The parietal P2 amplitude was reduced in response to negative NP trials. (4) Inhibition function was negatively correlated with rumination. (5) Both depressed patients and normal controls showed longer time in response to positive and negative NP targets in NAP task with degraded target stimuli. Participants for both groups showed increased LPC amplitude in response to positive and negative NP trials. The depressed patients showed larger LPC difference amplitude in response to negative NP trials than normal controls, however, normal controls showed larger LPC difference amplitude in response to positive NP trials than depressed patients.Conclusions: (1) A less effective inhibition is specific for negative information and not observed for positive information in depressed patients and remitted depressed individuals. Impaired inhibition of negative affect might be a cognitive vulnerability factor explaining depression. (2) The inhibition dysfunction of negative affect influences the earlier attention allocation stage and the later evaluation stage in depressed patients. (3) Inhibition function and rumination are important predictor for depression. (4) Depressed patients have intact automatic retrieval processes. (5) The consistency of behavioral and ERP data supports dual mechanisms of negative priming.