Anxiety disorders are common and have significant impacts on daily life and health. Recent neuroimaging research has focused on identifying the brain circuits underlying these disorders. Studies on fear circuits in animals and brain responses to emotional stimuli in humans have provided insights into the neurocircuitry of anxiety disorders. Research has shown heightened amygdala activation in response to disorder-relevant stimuli in post-traumatic stress disorder (PTSD), social phobia, and specific phobia. Activation in the insular cortex is also heightened in many anxiety disorders. PTSD is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex. Further research is needed to clarify the role of each component of the fear circuitry, determine whether functional abnormalities are acquired signs or risk factors, link neuroimaging findings with neurochemistry, and use neuroimaging to predict treatment response. The neurocircuitry of fear involves the amygdala, nucleus accumbens, hippocampus, ventromedial hypothalamus, periaqueductal gray, brainstem nuclei, thalamic nuclei, insular cortex, and prefrontal regions. These regions play roles in threat perception, fear learning, and response modulation. Key findings from animal studies, such as the role of the amygdala in fear conditioning and the involvement of the hippocampus in contextual processing, have been replicated across studies. These findings suggest similar functions in humans. In humans, fear conditioning involves the amygdala, dACC, and rACC, and is associated with increased activation in the insular cortex and hippocampus. Extinction learning involves the vmPFC, and amygdala and insular cortex activation may occur during extinction. Pharmacological challenges, such as CCK-4 and procaine, have shown increased amygdala and insular cortex activation in response to fear and anxiety. Emotional stimuli activate the amygdala, medial prefrontal cortex, and insular cortex, with the amygdala responding to emotionally arousing stimuli. Emotional facial expressions activate the amygdala, dACC, rACC, medial frontal gyrus, and insular cortex. The amygdala is activated by fear expressions, and its activation is associated with increased fear responses. The medial prefrontal cortex and insular cortex are involved in processing emotional stimuli and self-referential processing. The insular cortex is responsive to aversive stimuli and internal sadness. Stress is closely linked to the neurocircuitry of fear and anxiety. The limbic-hypothalamic-pituitary-adrenal (LHPA) axis is involved in stress responses and is linked to anxiety disorders. Stress can modulate fear responses, with differential effects in men and women. Chronic stress can impair extinction learning and alter fear conditioning. Stress exposure during development can affect fear/anxiety responses later in life. Anxiety disorders, including PTSD and panic disorder, involve hyperresponsivityAnxiety disorders are common and have significant impacts on daily life and health. Recent neuroimaging research has focused on identifying the brain circuits underlying these disorders. Studies on fear circuits in animals and brain responses to emotional stimuli in humans have provided insights into the neurocircuitry of anxiety disorders. Research has shown heightened amygdala activation in response to disorder-relevant stimuli in post-traumatic stress disorder (PTSD), social phobia, and specific phobia. Activation in the insular cortex is also heightened in many anxiety disorders. PTSD is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex. Further research is needed to clarify the role of each component of the fear circuitry, determine whether functional abnormalities are acquired signs or risk factors, link neuroimaging findings with neurochemistry, and use neuroimaging to predict treatment response. The neurocircuitry of fear involves the amygdala, nucleus accumbens, hippocampus, ventromedial hypothalamus, periaqueductal gray, brainstem nuclei, thalamic nuclei, insular cortex, and prefrontal regions. These regions play roles in threat perception, fear learning, and response modulation. Key findings from animal studies, such as the role of the amygdala in fear conditioning and the involvement of the hippocampus in contextual processing, have been replicated across studies. These findings suggest similar functions in humans. In humans, fear conditioning involves the amygdala, dACC, and rACC, and is associated with increased activation in the insular cortex and hippocampus. Extinction learning involves the vmPFC, and amygdala and insular cortex activation may occur during extinction. Pharmacological challenges, such as CCK-4 and procaine, have shown increased amygdala and insular cortex activation in response to fear and anxiety. Emotional stimuli activate the amygdala, medial prefrontal cortex, and insular cortex, with the amygdala responding to emotionally arousing stimuli. Emotional facial expressions activate the amygdala, dACC, rACC, medial frontal gyrus, and insular cortex. The amygdala is activated by fear expressions, and its activation is associated with increased fear responses. The medial prefrontal cortex and insular cortex are involved in processing emotional stimuli and self-referential processing. The insular cortex is responsive to aversive stimuli and internal sadness. Stress is closely linked to the neurocircuitry of fear and anxiety. The limbic-hypothalamic-pituitary-adrenal (LHPA) axis is involved in stress responses and is linked to anxiety disorders. Stress can modulate fear responses, with differential effects in men and women. Chronic stress can impair extinction learning and alter fear conditioning. Stress exposure during development can affect fear/anxiety responses later in life. Anxiety disorders, including PTSD and panic disorder, involve hyperresponsivity