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Variants within the GABA transaminase (ABAT) gene region are associated with somatosensory evoked EEG potentials in families at high risk for affective disorders

Published online by Cambridge University Press:  09 January 2012

M. Wegerer ,
S. Adena ,
A. Pfennig ,
D. Czamara ,
U. Sailer ,
T. Bettecken ,
B. Müller-Myhsok ,
S. Modell  and
M. Ising
M. Wegerer
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany Faculty of Psychology, University of Vienna, Vienna, Austria
S. Adena
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany
A. Pfennig
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany
D. Czamara
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany
U. Sailer
Affiliation:
Faculty of Psychology, University of Vienna, Vienna, Austria
T. Bettecken
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany
B. Müller-Myhsok
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany
S. Modell
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany
M. Ising*
Affiliation:
Max Planck Institute of Psychiatry, Munich, Germany
*
*Address for correspondence: M. Ising, Dr.Phil., Max Planck Institute of Psychiatry, Kraepelinstraße 2–10, 80804 Munich, Germany. (Email: ising@mpipsykl.mpg.de)
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Abstract

Background

Depression frequently co-occurs with somatization, and somatic complaints have been reported as a vulnerability marker for affective disorders observable before disease onset. Somatization is thought to result from an increased attention to somatic sensations, which should be reflected in long-latency somatosensory evoked electroencephalogram (EEG) potentials (SSEPs) at the physiological level. Previous studies revealed that SSEPs are altered in depressed patients and suggested late SSEP components as vulnerability markers for affective disorders. Neurotransmitters such as serotonin, γ-aminobutyric acid (GABA) and the neuropeptide substance P may play an important role for both affective disorders and somatosensory processing.

Method

We investigated the associations between SSEPs and polymorphisms within candidate genes of the serotonergic, GABAergic as well as the substance P system in subjects at high risk for affective disorders. The sample was composed of high-risk families participating in the Munich Vulnerability Study and genetic association analyses were calculated using qfam (family-based association tests for quantitative traits) implemented in PLINK 1.05.

Results

We observed significant associations (false discovery rate <0.05) withstanding correction for multiple testing between late SSEP components (response strength 170–370 ms after stimulation) and four single nucleotide polymorphisms within the GABA transaminase (ABAT) gene region coding for a protein responsible for GABA degradation. No effects were found with the classical disease trait approach, suggesting SSEP marker specificity of the observed associations.

Conclusions

Our findings point to a possible role of ABAT gene-regulated GABA catabolism for an altered processing of somatosensory stimuli as a potential vulnerability marker for affective disorders.

Keywords

Affective disordersdepressionGABA transaminasegeneticssomatizationsomatosensory evoked potentials
Type
Original Articles
Information
Psychological Medicine , Volume 43 , Issue 6 , June 2013 , pp. 1207 - 1217
Copyright
Copyright © Cambridge University Press 2012 

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Supplementary material: PDF

Wegerer Supplementary Table

Supplemental Online Table. SNP-characteristics and associations with SSEP parameters

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