This applied to patients with psychotic and nonpsychotic depression. The relation between PSDEP and NE was particularly present in patients with PSDEP and melancholia. Correlation between plasma norepinephrine and vasopressin in psychotic depression Figure 1 shows the uncorrected positive correlations between plasma NE and lnAVP in PSDEP and non-PSDEP. Partial

correlations between NE and lnAVP were analysed in the subgroups of PSDEP (n = 9) and non-PSDEP (n = 69), and in the subgroups of melancholic PSDEP (N = 7) and all other patients (N = 71), controlling for the Inhibitors,research,lifescience,medical effects of smoking habit, tricyclic treatment and antipsychotic drug dosage. These analyses showed positive correlations Inhibitors,research,lifescience,medical in both psychotic groups (r = 0.729 and r = 0.718 respectively), and the absence of a correlation in the two patient control groups (r = 0.050 and r = 0.049). Fisher’s z test showed that these correlations differed significantly in both comparisons (z = 4.11, p < 0.01; z = 3.32; p < 0.01). Figure 1. Relations between plasma norepinephrine and vasopressin (lnAVP). Discussion Increased noradrenergic activation in psychotic depression This study confirmed the hypothesis that PSDEP is characterized by an increased concentration of plasma NE, and reconfirmed the correlation between plasma NE and AVP concentrations [Goekoop et al. 2011] while Inhibitors,research,lifescience,medical using a more complete set of confounders in the analyses. The correlation between central and

plasma NE [Esler et al. 1995; Kelly and Cooper, 1997; Ziegler et al. 1977] suggests that in PSDEP a high central noradrenergic activation may induce a high noradrenergic–vasopressinergic activation. The role of NE and AVP in the activation of the HPA axis [Al-Damluji, Inhibitors,research,lifescience,medical 1993] suggests that an increased noradrenergic–vasopressinergic mechanism combined with the increased vasopressinergic activation of the HPA axis common to all depressive disorders [Goekoop et al. 2010] could explain the very high rate of dexamethasone nonsuppression that characterizes PSDEP [Nelson and Davis, 1997]. This hypothesis should be tested Inhibitors,research,lifescience,medical in future studies. The role of confounders The search for potential confounders appeared to be very useful in this study.

As far as the subcategories of depression are concerned, neither melancholia according to the selleck products DSM-IV-TR nor the better validated HAR and ANA subcategories appeared to be significantly related to PSDEP, and only the HAR subcategory was (negatively) related to plasma NE. In contrast, all three Megestrol Acetate global dimensions of the CPRS [Goekoop et al. 1992] selected for the study eventually appeared to be related to NE. The dimension of Emotional Dysregulation was negatively related, and the dimensions of Retardation and Anxiety positively related, as has been found previously [Roy et al. 1985b]. In separate analyses PSDEP appeared to be related to the dimension of (psychomotor) Retardation, evidence of which has also been found previously [Parker et al.