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Neurobiological correlates of social anxiety disorder: an update

  • Donatella Marazziti (a1), Marianna Abelli (a1), Stefano Baroni (a1), Barbara Carpita (a1), Carla E. Ramacciotti (a1) and Liliana Dell'Osso (a1)...
Abstract

Social anxiety disorder (SAD) is a condition characterized by pervasiveness and impairment in social functioning, with a prevalence in the general population between 1.9% and 12.1%. The most consistent findings on its neurobiological underpinnings involve a wide range of neurotransmitters (serotonin, norepinephrine, glutamate, and GABA) and neuropeptides (oxytocin), but no comprehensive hypothesis is yet available. In particular, oxytocin is becoming increasingly established as a “prosocial neuropeptide” and, as such, is a major focus of current research, with a great range of therapeutic applications including SAD treatment. Specifically, the amygdala plays a pivotal role in conditioning and processing of fear, and exaggerated amygdala responses in SAD patients have been observed during various social-emotional stimuli. In addition to the amygdala, other brain areas of interest in SAD-related circuitry are represented by the medial prefrontal cortex, dorsal raphe, striatum, locus coeruleus, prefrontal cortex, insular cortex, and anterior cingulate cortex. The aim of this review is to provide an update on neurobiological correlates of SAD, with a special focus on neurotransmitters and brain areas possibly involved, and suggestions for future research that could lead to more specific therapeutic interventions.

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Corresponding author
*Address for correspondence: Donatella Marazziti, MD, Dipartimento di Medicina Clinica e Sperimentale Section of Psychiatry, University of Pisa, Via Roma 67, Pisa 56100, Italy. (Email: dmarazzi@psico.med.unipi.it)
References
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