Neurobiological aspects of social anxiety disorder

Isr J Psychiatry Relat Sci. 2009;46(1):5-12.

Abstract

Social anxiety disorder (SAD) has in recent years been widely recognized as a major public health concern. Neurobiologically oriented studies could provide important clues to the causes and cures of this disorder. The present article addresses important findings from neuroimaging and other biological examinations of SAD. Aberrant patterns of brain activity in the amygdala/medial temporal lobe region, insula and striatum are suggested. There is also evidence of abnormalities in the serotonergic and dopaminergic transmission systems. Brain imaging studies have reported reduced serotonin-1A and dopamine D2 receptor binding in certain regions. It is also suggested that serotonin-related gene polymorphisms are important for amygdala responsivity and treatment outcome in SAD.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amygdala / physiopathology
  • Arousal / physiology
  • Brain / physiopathology*
  • Brain Mapping
  • Dopamine / physiology
  • Fear / physiology
  • Hippocampus / physiopathology
  • Humans
  • Neural Pathways / physiopathology
  • Phobic Disorders / genetics
  • Phobic Disorders / physiopathology*
  • Polymorphism, Genetic / genetics
  • Receptor, Serotonin, 5-HT1A / physiology
  • Receptors, Dopamine D2 / physiology
  • Serotonin / physiology
  • Serotonin Plasma Membrane Transport Proteins / genetics
  • Synaptic Transmission / physiology

Substances

  • Receptors, Dopamine D2
  • SLC6A4 protein, human
  • Serotonin Plasma Membrane Transport Proteins
  • Receptor, Serotonin, 5-HT1A
  • Serotonin
  • Dopamine