The neurobiology of social anxiety disorder is poorly understood, although preliminary research has suggested several possible biological abnormalities. Challenge studies have demonstrated that subjects with social anxiety disorder have a sensitivity to carbon dioxide, cholecystokinin, and caffeine somewhere between that of panic disorder patients and normal controls. Serotonergic pathways may play a role in social anxiety disorder, as shown by the clinical effectiveness of selective serotonin reuptake inhibitors, plus fenfluramine and m-chlorophenylpiperazine challenge studies. Dopaminergic function and striatal dopamine uptake appear to be reduced in social anxiety disorder. There is also evidence for cardiovascular and adrenergic abnormalities. Recently, positron emission tomography has begun to identify brain regions that appear to be uniquely activated in this condition. These results offer the promise of an understanding of the brain mechanisms of social anxiety disorder, but much further research is needed to fully elucidate the neurobiological cause(s) that exist.