Abstract
The allocation of attention modulates negative emotional processing in the amygdala. However, the role of passive exposure time to emotional signals in the modulation of amygdala activity during active task performance has not been examined. In two functional Magnetic Resonance Imaging (fMRI) experiments conducted in two different groups of healthy human subjects, we examined activation in the amygdala due to cued anticipation of painful stimuli while subjects performed a simple continuous performance task (CPT) with either a fixed or a parametrically varied trial duration. In the first experiment (N = 16), engagement in the CPT during a task with fixed trial duration produced the expected attenuation of amygdala activation, but close analysis suggested that the attenuation occurred during the period of active engagement in CPT, and that amygdala activity increased proportionately during the remainder of each trial, when subjects were passively exposed to the pain cue. In the second experiment (N = 12), the duration of each trial was parametrically varied, and we found that amygdala activation was linearly related to the time of passive exposure to the anticipatory cue. We suggest that amygdala activation during negative anticipatory processing depends directly on the passive exposure time to the negative cue.
Highlights
Seminal experiments in animals have identified the neurobiological basis of the conditioned fear response, i.e., freezing behavior and associated autonomic and endocrine responses in relation to anticipation of a fear-arousing stimulus [1,2]
To test the first hypothesis, we performed ROI analysis within bilateral amygdala and compared amygdala activation during anticipation of painful heat while subjects were engaged in the continuous performance task (CPT) (+CPT) to activation during anticipation of painful heat while subjects were not engaged in the CPT (-CPT) (Fig. 1A)
We examined the hypothesis that differential anticipatory amygdala activation between +CPT and –CPT conditions is powered by the actual engagement in the task (Fig. 1A)
Summary
Seminal experiments in animals have identified the neurobiological basis of the conditioned fear response, i.e., freezing behavior and associated autonomic and endocrine responses in relation to anticipation of a fear-arousing stimulus [1,2]. The lateral and central nuclei of the amygdala play a pivotal role in this process by activating: (1) the periaqueductal gray matter (PAG) to elicit immobility, (2) the lateral hypothalamus to induce autonomic arousal, and (3) the paraventricular nucleus of the hypothalamus to activate adaptive endocrine responses. This brain network underlies the so-called ‘‘passive fear reactions’’. During active coping some attentional resources are diverted away from the fear-arousing stimulus to the active motor task
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