MK4MDD

Study Report

Reference
CitationHolmes, 2010 PubMed
Full InfoHolmes, A.J., Bogdan, R. and Pizzagalli, D.A. (2010) Serotonin transporter genotype and action monitoring dysfunction: a possible substrate underlying increased vulnerability to depression. Neuropsychopharmacology, 35, 1186-1197.

Study
Hypothesis or Background A variable number of tandem repeats (short (S) vs long (L)) in the promoter region of the serotonin transporter gene (5-HTTLPR) and a functional variant of a single-nucleotide polymorphism (rs25531) in 5-HTTLPR have been recently associated with increased risk for major depressive disorder (MDD). In particular, relative to L/L or L(A) homozygotes (hereafter referred to as L' participants), S carriers or L(g)-allele carriers (S' participants) have been found to have a higher probability of developing depression after stressful life events, although inconsistencies abound. Previous research indicates that patients with MDD are characterized by executive dysfunction and abnormal activation within the anterior cingulate cortex (ACC), particularly in situations requiring adaptive behavioral adjustments following errors and response conflict (action monitoring). The goal of this study was to test whether psychiatrically healthy S' participants would show abnormalities similar to those of MDD subjects.
Sample Information19 S' and 14 L' participants
Method DetailTo this end, 19 S' and 14 L' participants performed a modified Flanker task known to induce errors, response conflict, and activations in various ACC subdivisions during functional magnetic resonance imaging.
Method Keywordsfunctional magnetic resonance imaging (fMRI)
ResultAs hypothesized, relative to L' participants, S' participants showed (1) impaired post-error and post-conflict behavioral adjustments; (2) larger error-related rostral ACC activation; and (3) lower conflict-related dorsal ACC activation.

Relationships reported by Holmes, 2010