Results: Analysis of covariance controlling for the effects of tr

Results: Analysis of covariance controlling for the effects of tricyclic antidepressant treatment (≥100 mg) and smoking habit showed that PSDEP had an increased concentration of plasma NE. The previously found correlation between plasma NE and AVP was still present after correcting for the effects of confounding variables. Conclusions: The results suggest an increased activity of the sympathetic nervous system in PSDEP that may act as a specific

mechanism for increased vasopressinergic activation. This supports the view of PSDEP as a distinct Inhibitors,research,lifescience,medical subcategory of major depression. Keywords: norepinephrine, psychotic depression, smoking, tricyclic antidepressant, vasopressin Introduction This study on norepinephrine (NE) in psychotic depression (PSDEP) is part of a series of investigations within the same patient sample that aimed to develop an improved differentiation of subcategories of depression, and to detect neurobiological markers of these subcategories and of depression at large. The neurobiological focus of these studies is on vasopressinergic mechanisms Inhibitors,research,lifescience,medical in depression [Goekoop et al. 2010] and its subcategories [Goekoop and Wiegant, 2009; Goekoop

et al. 2011]. The present study tests if PSDEP is characterized by a specifically high Inhibitors,research,lifescience,medical noradrenergic activation next to the increased noradrenergic–vasopressinergic coupling, selleck compound evidence of which has been found previously in a comparison with non-PSDEP [Goekoop et al. 2011]. We hypothesized the plasma concentration of NE to be increased as a mechanism associated with the positively correlating plasma vasopressin (AVP) and NE concentrations

in PSDEP [Goekoop et al. 2011]. The potential role of increased release of NE next to the increased NE–AVP correlation in Inhibitors,research,lifescience,medical PSDEP may be seen Inhibitors,research,lifescience,medical in the context of the vasopressinergic mechanisms in animal models of depression [Aguilera et al. 2008; Landgraf, 2006] and noradrenergic mechanisms involved in the hypothalamus–pituitary–adrenal (HPA) axis. The role of NE in stimulating the HPA axis has been studied extensively [Al-Damluji, 1993]. In human subjects noradrenergic agents stimulate the release of adrenocorticotroph hormone (ACTH) via an α-1 receptor in the brain at the level of the paraventricular nucleus (PVN) tuclazepam of the hypothalamus, and not at the peripheral level of the pituitary [Al-Damluji, 1993]. Though such noradrenergic stimulation of the PVN in rats and mice involves the synthesis of both corticotropin-releasing hormone [Day et al. 1999] and AVP in the parvocellular neurons [Vacher et al. 2002], the resulting release of ACTH depends particularly on the release of AVP [Al-Damluji, 1993]. We hypothesize that the increased noradrenergic activation suggested by the correlating plasma NE and AVP concentrations in PSDEP involves a centrally increased release of plasma NE. The correlation between central and plasma NE [Esler et al. 1995; Kelly and Cooper, 1997; Ziegler et al.

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