How the serotonin transporter 5-HTTLPR polymorphism influences amygdala function: The roles of in vivo serotonin transporter expression and amygdala structure

Publikation: Beitrag in FachzeitschriftForschungsartikelBeigetragenBegutachtung

Beitragende

  • A. Kobiella - , Technische Universität Dresden, Universität Heidelberg (Autor:in)
  • M. Reimold - , Eberhard Karls Universität Tübingen (Autor:in)
  • D. E. Ulshöfer - , Universität Heidelberg (Autor:in)
  • V. N. Ikonomidou - , George Mason University (Autor:in)
  • C. Vollmert - , Universität Heidelberg (Autor:in)
  • S. Vollstädt-Klein - , Universität Heidelberg (Autor:in)
  • M. Rietschel - , Universität Heidelberg (Autor:in)
  • G. Reischl - , Eberhard Karls Universität Tübingen (Autor:in)
  • A. Heinz - , Charité – Universitätsmedizin Berlin (Autor:in)
  • M. N. Smolka - , Klinik und Poliklinik für Psychiatrie und Psychotherapie, Neuroimaging Center (Autor:in)

Abstract

The serotonin transporter-linked promoter region (5-HTTLPR) polymorphism of the serotonin transporter gene is associated with amygdala response during negative emotion. The aim of this study was to investigate whether this genotype effect on amygdala function is mediated by current serotonin transporter (5-HTT) levels or rather by genetically induced influences during neurodevelopment, shaping brain structure. A total of 54 healthy subjects underwent functional and structural magnetic resonance imaging, 11 CDASB positron emission tomography and 5-HTTLPR genotyping to analyze the interrelationships between amygdala activation during processing of unpleasant stimuli, 5-HTTLPR genotype, amygdala volumes and 5-HTT levels in the midbrain and in other brain regions. In line with previous research, carriers of the short allele (S) showed increased amygdala activation. Path analysis demonstrated that this genotype effect was not procured by current 5-HTT availability but by amygdala structure, with smaller amygdala volumes in the S than in the LL genotype, as well as smaller volumes being associated with increased amygdala activation. Our findings stress the role of genetic effects during neurodevelopment.

Details

OriginalspracheEnglisch
Aufsatznummere37
FachzeitschriftTranslational psychiatry
Jahrgang1
PublikationsstatusVeröffentlicht - 2011
Peer-Review-StatusJa

Externe IDs

PubMed 22832611
ORCID /0000-0001-5398-5569/work/161890841

Schlagworte

Schlagwörter

  • 5-HTT, 5-HTTLPR, [11C]DASB PET, amygdala, fMRI, structural MRI