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

• Published in: Psychological medicine Vol. 43; no. 6; pp. 1207 - 1217
• Main Authors: Wegerer, M., Adena, S., Pfennig, A., Czamara, D., Sailer, U., Bettecken, T., Müller-Myhsok, B., Modell, S., Ising, M.
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 01.06.2013
• Subjects: 3' Untranslated Regions; 4-Aminobutyrate Transaminase - genetics; Adult; Adult and adolescent clinical studies; Affective disorders; Biological and medical sciences; Brain; Depression; Electroencephalography; Emotional disorders; Evoked Potentials, Somatosensory - genetics; Family medical history; Female; Gamma-aminobutyric acid; Genes; Genetic Predisposition to Disease; High risk; Humans; Information processing; Male; Medical sciences; Middle Aged; Mood disorders; Mood Disorders - enzymology; Mood Disorders - genetics; Mood Disorders - psychology; Neurotransmitters; Original Articles; Polymorphism, Single Nucleotide; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Somatization; Somatoform Disorders - genetics; Somatoform Disorders - psychology; Somatoform disorders. Psychosomatics; Vulnerability; GABA transaminase; genetics; depression; Affective disorders; somatization; somatosensory evoked potentials; Social environment; Mood disorder; High risk; 4-Aminobutyrate transaminase; Enzyme; Transferases; Electrophysiology; Somatization; Depression; Electroencephalography; Genetic determinism; Affective disorder; Electrodiagnosis; Gene; Transaminases; Somatoform disorder; Risk factor; Family environment; Genetics; Somatosensory evoked potential
• ISSN: 0033-2917; 1469-8978
• DOI: 10.1017/S0033291711002923

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. 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. 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.