Increased Number of Vasopressin- and Oxytocin-Expressing Neurons in the Paraventricular Nucleus of the Hypothalamus in Depression

Abstract

The AVP and OXT neurons were activated in the PVN in patients with major depression or bipolar disorder. This activation may be associated with activation of the hypothalamic-pituitary-adrenal axis in these patients, since both AVP and OXT are known to potentiate the effects of corticotropin-releasing hormone. Because of their central effects, activation of AVP and OXT neurons may also be related to symptoms of major depression or bipolar disorder.

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

“…This altered feedback might be involved in adaptive changes described post mortem in the hypothalamic CRH and AVP neurons that control the pituitary-adrenocortical system (Purba et al 1996). Thus, the HAB animals may represent a promising model for further investigation of the psychopathological significance of a dysregulated HPA system.…”

“…Thus, the hypothalamic signal for ACTH secretion produced by the parvocellular CRH neurons gradually shifts from a CRH-dominated signal to a more AVP-dominated one . Indeed, Purba et al (1996) found indications of an enhanced vasopressinergic drive by showing an increased number of AVP-expressing neurons in the PVN of depressed patients. Although the findings so far are not consistent (Heuser et al 1998), additional indirect evidence for a role of AVP in affective disorders comes from the finding that fluoxetine treatment leads to a reduction in cerebrospinal fluid concentrations of AVP in patients with major depression (de Bellis et al 1993).…”

“…The effects of CRH are modulated by vasopressin (AVP), which, after prolonged stress and in senescence, is increasingly coexpressed and secreted from hypothalamic CRH neurons in both humans and rodents (Antoni 1993;Tilders et al 1993;Hatzinger et al 2000;Keck et al 2000). Similarly, increased numbers of CRH neurons that coexpress AVP mRNA have been found in the hypothalamus of depressed patients (Raadsheer et al 1993;Purba et al 1996). The excessive release of CRH and AVP into hypophysial portal blood is thought to increase the secretion of corticotropin (ACTH) from pituitary corticotrope cells, and this in turn to increase the release of corticosteroids from the adrenal gland.…”

“…The CRH/AVP synergism is known to be functionally relevant under conditions of long-term activation of the HPA system, such as chronic stress in rats (e.g. de Goeij et al 1992), human and rodent aging (Lucassen et al 1993;Hatzinger et al 2000;Keck et al 2000) and human depression (Holsboer 1999;Purba et al 1996). Thus, the hypothalamic signal for ACTH secretion produced by the parvocellular CRH neurons gradually shifts from a CRH-dominated signal to a more AVP-dominated one .…”

Restoration of peripheral V2 receptor vasopressin signaling fails to correct behavioral changes in Brattleboro rats

“…Clinical studies found an increased AVP concentration in the cerebrospinal fluid (De Bellis et al, 1993, Heuser et al, 1998 and in the plasma (van Londen et al, 1997, van Londen et al, 1998, de Kloet et al, 2008 of depressive subjects, especially in suicide victims (Inder et al, 1997, Brunner et al, 2002. Postmortem studies have found an elevated number of AVP-expressing neurons, increased AVP level in the PVN (Purba et al, 1996, Merali et al, 2006 and an enhanced AVP mRNA You created this PDF from an application that is not licensed to print to novaPDF printer (http://www.novapdf.com) in the SON (Meynen et al, 2006). Additionally, a single nucleotide polymorphism of the AVP V1b receptor has been found to protect against major depression (van West et al, 2004).…”