Neuroimaging studies using PET and SPECT to evaluate neurofunctional differences in the brain between patients with anxiety disorders and healthy controls were reviewed. At rest patients with social anxiety disorder display a reduced dopamine-D2 receptor binding potential. Post-traumatic stress disorder is associated with a compromised benzodiazepine receptor function. In panic disorder, both benzodiazepine receptors and serotonergic (5-hydroxytryptamine 1A; 5HT 1A) receptors are downregulated. Across the anxiety disorders there is downregulation of both benzodiazepine and 5HT 1A receptors. Symptom provocation studies, where regional cerebral blood fl ow is measured, support that activity in the brain’s fear circuit is altered with increased reactivity in the amygdala, the midbrain and possibly also the insula cortex, whereas activity in emotionregulating areas in the prefrontal cortex such as the subgenual anterior cingulate cortex and the orbitofrontal cortex is compromised in the symptomatic state, predominantly in phobic disorders. Some studies demonstrate a coupling between individual differences in neurotransmission and fear network activity. Treatment studies suggest that reductions of neural activity in the amygdala may be a fi nal common pathway for successful therapeutic interventions, thereby linking neurotransmission to plasticity in the core fear network of the brain.