A major SNP haplotype of the arginine vasopressin 1B receptor protects against recurrent major depression

West, Dirk Van; Del-Favero, Jurgen; Aulchenko, Yurii S.; Oswald, Pierre; Souery, Daniel; Forsgren, T; Sluijs, S; Belkacem, Sabrina; Adolfsson, Rolf; Mendlewicz, Julien; Duijn, Cornelia M. van; Deboutte, Dirk; Broeckhoven, Christine Van; Claes, Stephan

doi:10.1038/sj.mp.4001420

Cited by 92 publications

(52 citation statements)

References 24 publications

(19 reference statements)

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“…34,75,76 It was also of interest to find single AR nuclear and/ or cytoplasmic staining inside the PVN in the human hypothalamus ( Figure 4) as this implicates a potential role of androgens on the activity of peptidergic neurons other than CRH neurons, for example the vasopressin or oxytocin-containing neurons, both of which are also involved in central stress responses and mood disorders. [77][78][79][80][81][82] This topic also deserves further study.…”

Section: Mmtv-arementioning

confidence: 99%

A direct androgenic involvement in the expression of human corticotropin-releasing hormone

Fischer

et al. 2006

Mol Psychiatry

104

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We investigated the possibility of a direct action of androgens on the expression of the human corticotropin-releasing hormone (CRH), which plays a central role in the hypothalamicpituitary-adrenal (HPA)-axis. Colocalization of CRH and nuclear/cytoplasmic androgen receptor (AR) was found in neurons of the paraventricular nucleus (PVN) in the human hypothalamus. A potential androgen-responsive element (ARE) in the human CRH promoter was subsequently analyzed with bandshifts and cotransfections in neuroblastoma cells. In the presence of testosterone, recombinant human AR bound specifically to the CRH-ARE. Expression of AR in combination with testosterone repressed CRH promoter activity through the ARE. We conclude that androgens may directly affect CRH neurons in the human PVN via AR binding to the CRH-ARE, which may have consequences for sex-specific pathogenesis of mood disorders.

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Section: Mmtv-arementioning

confidence: 99%

A direct androgenic involvement in the expression of human corticotropin-releasing hormone

Fischer

et al. 2006

Mol Psychiatry

104

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“…This paper is a part of a systematic evaluation of the possible role of a number of HPA axis-related genes in the genetic vulnerability for MDD. Previously, our group published reports on the genes encoding for the CRF receptor 2, the CRF binding protein, and the AVP receptor 1B (Claes et al, 2003;van West et al, 2004;Villafuerte et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid Receptor Gene-Based SNP Analysis in Patients with Recurrent Major Depression

West

Eede

Del-Favero

et al. 2005

Neuropsychopharmacol

136

108

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Dysregulation of the hypothalamic-pituitary-adrenal axis, one of the stress-response systems, is one of the key neurobiological features of major depression (MDD). Data supporting the notion that glucocorticoid-mediated feedback inhibition is impaired in MDD come from a multitude of studies demonstrating nonsuppression of cortisol secretion following administration of the synthetic glucocorticoid dexamethasone. We examined whether genetic variations in the glucocorticoid receptor gene (Nuclear Receptor Subfamily 3, Group C, Member 1; NR3C1) could be associated with increased susceptibility for MDD using a whole gene-based association analysis of single nucleotide polymorphisms (SNPs). Four SNPs were identified in NR3C1 and genotyped in two well-diagnosed samples of patients with MDD ascertained in Belgium and northern Sweden, and matched control samples. In total, 314 MDD patients and 354 control individuals were included in the study. In the Belgian sample, we observed significant allele (p ¼ 0.02) and genotype (p ¼ 0.02) association with an SNP in the promoter region (NR3C1-1); in the Swedish sample, we observed significant allele (p ¼ 0.02) and genotype (p ¼ 0.02) association with the R23K SNP. The haplotype association studies showed modest evidence for an involvement of the 5 0 region of the NR3C1 gene in the genetic vulnerability for MDD. This study suggests that polymorphisms in the 5 0 region of the NR3C1 gene may play a role in the genetic vulnerability for MDD.

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“…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). Preclinical studies using the first orally active non-peptide V1b antagonist (SSR 149415) resulted in a reduction of floating in the FS test (Griebel et al, 2002).…”

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confidence: 99%

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

Balázsfi

Pintér

Klausz

et al. 2015

Psychoneuroendocrinology

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Short title:Stress-related behavior in Brattleboro rat after DDAVP treatment You created this PDF from an application that is not licensed to print to novaPDF printer (http://www.novapdf.com) Balázsfi et al. 2Highlights  The effect of AVP on affective and memory symptoms is due to its central role  DDAVP treatment compensated the peripheral effects of congenital AVP absence  DDAVP did not significantly alter the behavior of KO animals in the paradigms tested  AVP signaling in the medial amygdala contributes to the behavioral effect measured in FS AbstractBeside its hormonal function in salt and water homeostasis, vasopressin -released into distinct brain areas -plays a crucial role in stress-related behavior resulting in the enhancement of an anxious/depressive-like state.We aimed to investigate whether correction of the peripheral symptoms of congenital absence of AVP also corrects the behavioral alterations in AVP-deficient Brattleboro rats. Wild type (WT) and vasopressin-deficient (KO) male Brattleboro rats were tested.Half of the KO animals were treated by desmopressin (V2-receptor agonist) via osmotic minipump (subcutaneous) to eliminate the peripheral symptoms of vasopressin-deficiency. Anxiety was studied by elevated plus maze (EPM), defensive withdrawal (DW) and marble burying (MB) tests, while depressive-like changes were monitored in forced swimming (FS) and anhedonia by sucrose preference test. Cell activity was examined in septum and amygdala by c-Fos immunohistochemistry after 10min FS.

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A major SNP haplotype of the arginine vasopressin 1B receptor protects against recurrent major depression

Cited by 92 publications

References 24 publications

A direct androgenic involvement in the expression of human corticotropin-releasing hormone

A direct androgenic involvement in the expression of human corticotropin-releasing hormone

Glucocorticoid Receptor Gene-Based SNP Analysis in Patients with Recurrent Major Depression

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

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