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Genotype over-diagnosis in amygdala responsiveness: affective processing in social anxiety disorder.

Artikel i vetenskaplig tidskrift
Författare Tomas Furmark
Susanne Henningsson
Lieuwe Appel
Fredrik Ahs
Clas Linnman
Anna Pissiota
Vanda Faria
Lars Oreland
Massimo Bani
Emilio Merlo Pich
Elias Eriksson
Mats Fredrikson
Publicerad i Journal of psychiatry & neuroscience : JPN
Volym 34
Nummer/häfte 1
Sidor 30-40
ISSN 1488-2434
Publiceringsår 2009
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi
Sidor 30-40
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adult, Amygdala, radionuclide imaging, Anxiety Disorders, genetics, psychology, radionuclide imaging, Emotions, Female, Gene Frequency, Genotype, Humans, Male, Middle Aged, Polymorphism, Genetic, genetics, Positron-Emission Tomography, Psychiatric Status Rating Scales, Serotonin Plasma Membrane Transport Proteins, genetics, Tryptophan Hydroxylase, genetics, Young Adult
Ämneskategorier Farmakologi och toxikologi


BACKGROUND: Although the amygdala is thought to be a crucial brain region for negative affect, neuroimaging studies do not always show enhanced amygdala response to aversive stimuli in patients with anxiety disorders. Serotonin (5-HT)-related genotypes may contribute to interindividual variability in amygdala responsiveness. The short (s) allele of the 5-HT transporter linked polymorphic region (5-HTTLPR) and the T variant of the G-703T polymorphism in the tryptophan hydroxylase-2 (TPH2) gene have previously been associated with amygdala hyperresponsivity to negative faces in healthy controls. We investigated the influence of these polymorphisms on amygdala responsiveness to angry faces in patients with social anxiety disorder (SAD) compared with healthy controls. METHODS: We used positron emission tomography with oxygen 15-labelled water to assess regional cerebral blood flow in 34 patients with SAD and 18 controls who viewed photographs of angry and neutral faces presented in counterbalanced order. We genotyped all participants with respect to the 5-HTTLPR and TPH2 polymorphisms. RESULTS: Patients with SAD and controls had increased left amygdala activation in response to angry compared with neutral faces. Genotype but not diagnosis explained a significant portion of the variance in amygdala responsiveness, the response being more pronounced in carriers of s and/or T alleles. LIMITATIONS: Our analyses were limited owing to the small sample and the fact that we were unable to match participants on genotype before enrollment. In addition, other imaging techniques not used in our study may have revealed additional effects of emotional stimuli. CONCLUSION: Amygdala responsiveness to angry faces was more strongly related to serotonergic polymorphisms than to diagnosis of SAD. Emotion activation studies comparing amygdala excitability in patient and control groups could benefit from taking variation in 5-HT-related genes into account.

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