Genotype-controlled analysis of serum dopamine β-hydroxylase activity in civilian post-traumatic stress disorder

Abstract

Background Norepinephrine (NE) plays a central role in post-traumatic stress disorder (PTSD). Dopamine β-hydroxylase (DβH) converts dopamine (DA) to NE and its activity varies widely across individuals. Mustapic et al. (2007) reported a PTSD-associated deficit in serum DβH activity in a genotype-controlled analysis of combat veterans. We tested whether such a deficit would occur in a sample of civilians. Methods The severity of current adult PTSD symptoms and current DSM-IV diagnosis of PTSD were determined by the PTSD Symptom Scale (PSS). Adulthood trauma exposure was assessed using the Traumatic Experience Inventory (TEI). Serum DβH activity (sDβH) was assayed by HPLC with electrochemical detection and genotypes were determined using the Taqman® platform. Results Two hundred and twenty seven African American (AA) subjects were enrolled in this study, with a mean age (± SD) of 42.9 (± 12.9) years. We found a strong association between rs1611115 genotype and sDβH (p < 0.0001). After controlling for adulthood trauma exposure, there were no significant differences of sDβH between subjects who met a PTSD diagnosis and those who did not (p > 0.05) in any genotype group. No significant correlations were found between sDβH and PTSD severity, but sDβH significantly associated with the status of comorbid depression based on the cutoff of HAMD (p = 0.014) in subjects with PTSD. Conclusions We have replicated in this sample the prior finding that DBH rs1611115 genotype strongly associates with sDβH. No associations between sDβH and PTSD diagnosis or symptom severity were found in this civilian sample.