Polymorphisms within the 4-aminobutyrate aminotransferase gene are associated with long-latency somatosensory potentials in families vulnerable for affective disorders

Abstract

Depression is known to frequently co-occur with somatic symptoms and data from the Munich Vulnerability Study pointed to somatization as a possible vulnerability marker for affective disorders observable before disease onset. In this context previous studies furthermore revealed long-latency somatosensory evoked potentials (SSEP) to be a potential marker for susceptibility to depressive disorder. Based on this evidence we performed a small family-based association study to investigate genetic associations between long-latency SSEP and polymorphisms within candidate gene regions of somatosensory pathways including the serotonergic, GABAergic as well as the substance P system. The sample was composed of families at high risk for affective disorders who were participating in the Munich Vulnerability Study. We observed significant associations between average SSEP response strength in the long-latency range and polymorphisms within the 3' untranslated region of the 4-aminobutyrate aminotransferase gene coding for a protein responsible for GABA degradation. These findings point to a possible role of GABA catabolism in processing of somatosensory stimuli as well as for bodily misperceptions in connection with vulnerability for affective disorders.