Figure 1.

Model for the neurocircuitry of fear regulation in humans through extinction, cognitive regulation, active coping, and reconsolidation. A network of structures including the amygdala, hippocampus, vmPFC, dlPFC, and the striatum are involved in the regulation of conditioned fear expression. The lateral nucleus (LA) of the amygdala receives afferent sensory input and is the site of CS–US plasticity during fear conditioning. The LA projects to the central nucleus (CE), which has outputs to regions that control the expression of the CR. Projections from the hippocampus to the basal nucleus (B) of the amygdala process contextual information during conditioning, and may gate fear expression through the CE. During extinction learning and consolidation, inhibitory connections between the vmPFC and the intercalated (ITC) cell masses are established. During extinction recall, these connections inhibit fear expression through projections to the CE. Inhibitory connections between the vmPFC and the LA may also regulate fear expression during extinction recall through the CE. Contextual modulation of extinction expression is mediated by projections from the hippocampus to the vmPFC and/or LA. During cognitive regulation, the dorsolateral prefrontal cortex (dlPFC) regulates fear expression through projections to the vmPFC, which in turn inhibits amygdala activity. During active coping, information from the LA is routed not to the CE, which drives fear expression, but to the B, which in turn projects to the striatum. The striatum is thought to reinforce instrumental action taken during escape-from-fear or avoidance learning. Reconsolidation diminishes conditioned fear expression through alteration of the original CS–US association stored in the LA.