1. ¹Department of Psychiatry, University of Münster, Münster, Germany
2. ²IZKF-Research Group 4, IZKF Münster, University of Münster, Münster, Germany
3. ³Department of Psychiatry, University of Würzburg, Würzburg, Germany
4. ⁴Department of Clinical Radiology, University of Münster, Münster, Germany
5. ⁵Department of Psychiatry, James Cook University, Townsville, QLD, Australia

Correspondence: Dr T Suslow, Department of Psychiatry, University of Münster, Albert-Schweitzer-Strasse 11, 48149 Münster, Germany. Tel: +49 251 835 6615; Fax: +49 251 835 6612; E-mail: Thomas.Suslow@ukmuenster.de

Received 15 November 2006; Revised 2 March 2007; Accepted 5 March 2007; Published online 4 April 2007.

Abstract

The amygdala is a key structure in a limbic circuit involved in the rapid and unconscious processing of facial emotions. Increased amygdala reactivity has been discussed in the context of major depression. Recent studies reported that amygdala activity during conscious emotion processing is modulated by a functional polymorphism in the serotonin transporter gene (5-HTTLPR) in healthy subjects. In the present study, amygdala reactivity to displays of emotional faces was measured by means of fMRI at 3T in 35 patients with major depression and 32 healthy controls. Conscious awareness of the emotional stimuli was prevented via backward-masking to investigate automatic emotion processing. All subjects were genotyped for the 5-HTTLPR polymorphism. Risk allele carriers (S or L_G) demonstrated increased amygdala reactivity to masked emotional faces, which in turn was significantly correlated with life-time psychiatric hospitalization as an index of chronicity. This might indicate that genetic variations of the serotonin transporter could increase the risk for depression chronification via altering limbic neural activity on a preattentive level of emotion processing.