5-HTT genotype effect on prefrontal-amygdala coupling differs between major depression and controls.
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5-HTT genotype effect on prefrontal-amygdala coupling differs between major depression and controls. / Friedel, Eva; Schlagenhauf, Florian; Sterzer, Philipp; Park, Soyoung Q; Bermpohl, Felix; Ströhle, Andreas; Stoy, Meline; Puls, Imke; Hägele, Claudia; Wrase, Jana; Büchel, Christian; Heinz, Andreas.
In: PSYCHOPHARMACOLOGY, Vol. 205, No. 2, 2, 2009, p. 261-271.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - 5-HTT genotype effect on prefrontal-amygdala coupling differs between major depression and controls.
AU - Friedel, Eva
AU - Schlagenhauf, Florian
AU - Sterzer, Philipp
AU - Park, Soyoung Q
AU - Bermpohl, Felix
AU - Ströhle, Andreas
AU - Stoy, Meline
AU - Puls, Imke
AU - Hägele, Claudia
AU - Wrase, Jana
AU - Büchel, Christian
AU - Heinz, Andreas
PY - 2009
Y1 - 2009
N2 - RATIONALE: In major depression, prefrontal regulation of limbic brain areas may be a key mechanism that is impaired during the processing of affective information. This prefrontal-limbic interaction has been shown to be modulated by serotonin (5-HTT) genotype, indicating a higher risk for major depressive disorder (MDD) with increasing number of 5-HTT low-expression alleles. OBJECTIVE: Functional magnetic resonance imaging was used to assess neural response to uncued unpleasant affective pictures in 21 unmedicated patients with MDD compared to 21 matched healthy controls, taking into account genetic influences of the 5-HTT (SCL6A4) high- and low-expression genotype. RESULTS: Healthy controls displayed greater prefrontal activation (BA10) to uncued negative pictures compared to patients with MDD. While in healthy controls prefrontal (BA10) activation and BA10-amygdala coupling increased with the number of 5-HTT low-expression risk alleles, this effect was abolished, and even reversed, in patients with MDD. In MDD, connectivity decreased with severity of depressive symptoms (HAMD total score). CONCLUSION: These findings suggest that increased medial prefrontal (BA10) activation and BA10-amygdala connectivity may counteract the risk for MDD in healthy carriers of 5-HTT low-expression alleles, while this protective factor might be lost in patients who actually suffer from MDD. Prefrontal-limbic regulation in risk populations could be a target of early interventions and should be the focus of further research.
AB - RATIONALE: In major depression, prefrontal regulation of limbic brain areas may be a key mechanism that is impaired during the processing of affective information. This prefrontal-limbic interaction has been shown to be modulated by serotonin (5-HTT) genotype, indicating a higher risk for major depressive disorder (MDD) with increasing number of 5-HTT low-expression alleles. OBJECTIVE: Functional magnetic resonance imaging was used to assess neural response to uncued unpleasant affective pictures in 21 unmedicated patients with MDD compared to 21 matched healthy controls, taking into account genetic influences of the 5-HTT (SCL6A4) high- and low-expression genotype. RESULTS: Healthy controls displayed greater prefrontal activation (BA10) to uncued negative pictures compared to patients with MDD. While in healthy controls prefrontal (BA10) activation and BA10-amygdala coupling increased with the number of 5-HTT low-expression risk alleles, this effect was abolished, and even reversed, in patients with MDD. In MDD, connectivity decreased with severity of depressive symptoms (HAMD total score). CONCLUSION: These findings suggest that increased medial prefrontal (BA10) activation and BA10-amygdala connectivity may counteract the risk for MDD in healthy carriers of 5-HTT low-expression alleles, while this protective factor might be lost in patients who actually suffer from MDD. Prefrontal-limbic regulation in risk populations could be a target of early interventions and should be the focus of further research.
M3 - SCORING: Zeitschriftenaufsatz
VL - 205
SP - 261
EP - 271
JO - PSYCHOPHARMACOLOGY
JF - PSYCHOPHARMACOLOGY
SN - 0033-3158
IS - 2
M1 - 2
ER -