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Patients with social anxiety disorder may have overactive presynaptic serotonin system
Results from positron emission tomography scans indicate patients with social anxiety disorder have invariably increased serotonin synthesis and transporter availability compared with healthy patients.
“The neural underpinnings of excessive social anxiety are not fully characterized, although serontnin (5- hydroxytryptamine) has been suggested to be involved etiologically,” study researcher Andreas Frick, MSc, of Uppsala University in Uppsala, Sweden, and colleagues wrote in JAMA Psychiatry. “Findings from molecular and functional neuroimaging and treatment studies indicate that serotonergic neurotransmission in the amygdala, raphe nuclei, striatum, thalamus, hippocampus, insula cortex, and [anterior cingulate cortex] may be compromised in [social anxiety disorder].”
Researchers used positron emission tomography (PET) to assess serotonin synthesis and serotonin transporter availability among 18 patients with social anxiety disorder (mean age, 32.6 years) and 18 healthy patients (mean age, 34.7 years).
Patients with social anxiety disorder had increased rates of serotonin synthesis in the amygdala, brainstem corresponding to the raphe nuclei region, caudate nucleus, putamen, hippocampus and dorsal anterior cingulate cortex compared with controls.
Compared with controls, patients with social anxiety disorder had significantly higher serotonin transporter availability in the brainstem corresponding to the raphe nuclei region, caudate nucleus, putamen, thalamus and insula.
Patients with social anxiety disorder had increased carbon-labeled 3-amino-4-(2-dimethylaminomethylphenylsulfanyl)-benzonitrile binding potential ([C11]DASB BP) in the right putamen (P = .003) and left thalamus (P = .02) compared with controls.
Social anxiety symptom scores were positively correlated with carbon 11-labeled 5-hydroxytryptophan ([C11]5-HTP) in the right amygdala (P = .001) and negatively associated with ([C11]DASB BP in the left dorsal anterior cingulate cortex (P = .02) among patients with social anxiety disorder.
“The findings by Frick et al point to a potentially novel disrupted regulatory sequence in serotonin neurochemistry resulting from overactive serotonin signaling and having aspects in common with other preclinical and human models of increased anxiety traits and behavior,” Murray B. Stein, MD, MPH, of the University of California, San Diego, and Anne M. Andrews, PhD, of the Hatos Center for Neuropharmacology, wrote in an accompanying editorial. “Larger replication studies, possibly using additional imaging ligands and modalities, will be valuable for further exploring these theories.” – by Amanda Oldt
Disclosure: Frick and colleagues report no relevant financial disclosures. Stein reports being a consultant for Pfizer, Janssen and Tonix Pharmaceuticals. Andrews reports being a consultant for Forest Laboratories.