Individual Differences in Trait Anxiety Predict the Response of the Basolateral Amygdala to Unconsciously Processed Fearful Faces

Abstract

Responses to threat-related stimuli are influenced by conscious and unconscious processes, but the neural systems underlying these processes and their relationship to anxiety have not been clearly delineated. Using fMRI, we investigated the neural responses associated with the conscious and unconscious (backwardly masked) perception of fearful faces in healthy volunteers who varied in threat sensitivity (Spielberger trait anxiety scale). Unconscious processing modulated activity only in the basolateral subregion of the amygdala, while conscious processing modulated activity only in the dorsal amygdala (containing the central nucleus). Whereas activation of the dorsal amygdala by conscious stimuli was consistent across subjects and independent of trait anxiety, activity in the basolateral amygdala to unconscious stimuli, and subjects' reaction times, were predicted by individual differences in trait anxiety. These findings provide a biological basis for the unconscious emotional vigilance characteristic of anxiety and a means for investigating the mechanisms and efficacy of treatments for anxiety.

Stop the sadness: Neuroticism is associated with sustained medial prefrontal cortex response to emotional facial expressions

“…In our sample the two facets were highly correlated (R 2 =.38, p<.01). Given the relationship between anxiety and the processing of fearful stimuli (Etkin et al, 2004;Rauch et al, 2003), a similar analysis using a sample of highly anxious and low depressed (as measured by neuroticism facets) individuals may yield insights into the possible relationship between neuroticism and sustained processing of fearful stimuli.…”

The association of anxiety disorders and obsessive compulsive personality disorder with anorexia nervosa: Evidence from a family study with discussion of nosological and neurodevelopmental implications

“…An area of research we believe to have particular relevance to our findings is the affective neuroscience perspective on motivated behavior, a literature that has strongly implicated dysfunction in neural circuits mediating anxiety and fear learning in a range of pathological anxiety states. Specifically, in both human and animals studies, a wide range of anxiety phenotypes have been linked to overactivity of the amygdala, a key structure mediating innate fear proneness and the acquisition of learned fear, and of the hippocampus, which mediates the organism's defensive adaptation to novelty and plays a critical role in emotional memory 21,[26][27][28] ; dysfunction in frontal systems that regulate amygdala activation by threatening stimuli 29,30 ; altered morphometry in brain areas underlying the regulation of anxiety and fear-related behaviors 29,[31][32][33][34][35] ; and specific genetic variants that moderate the engagement of these circuits by threat stimuli. 36 Accordingly, behavioral manifestations of amygdaloid and hippocampal structures that are hypersensitive, or abnormally modulated-biased attention to novelty and threat, inhibition of appetitive behavior upon confrontation by novel or aversive environments, enhancement of fear learning, and poor retention of fear extinction (see Gray and McNaughton, 21 and Lang et al 22 for background)-may be a heuristic framework for exploring genetic and neurobiological underpinnings of the anxious premorbid temperament and anxiety-related diagnostic features of AN.…”

COMT genotype influences prefrontal response to emotional distraction

“…In contrast to earlier work, in which the activity of typical or average brains (Posner & Raichle, 1995) or differences between normal and pathological brains (Frith & Dolan, 1998) were mapped, in recent studies correlations have been made between differences in brain activity during cognitive or affective processing and normal individual variation in characteristics such as intelligence (Gray, Chabris, & Braver, 2003), anxiety (Bishop, Duncan, Brett, & Lawrence, 2004;Etkin et al, 2004), extraversion, and neuroticism (Canli, Silvers, Whitfield, Gotlib, & Gabrieli, 2002;Canli et al, 2001).…”