Corticotropin-Releasing Hormone, Arginine Vasopressin, Gastrin-Releasing Peptide, and Neuromedin B Alterations in Stress-Relevant Brain Regions of Suicides and Control Subjects

Merali, Zul; Kent, Pamela; Du, Lisheng; Hrdina, Pavel D.; Palkovits, Miklós; Faludi, Gábor; Poulter, Michael O.; Bédard, Tania; Anisman, Hymie

doi:10.1016/j.biopsych.2005.08.008

Cited by 140 publications

(73 citation statements)

References 97 publications

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“…This confirms our earlier studies in depressed patients with other techniques, showing an increase in the number of CRF-immunopositive neurons in depression 4,28 and elevated levels of CRF mRNA as determined by in situ hybridization. 5 So far, only one related study 45 on brain tissue in suicide victims has been carried out in which no significant increase of CRF mRNA in the PVN was found. However, in the study, the concentration of CRF was measured in a PVN punch and not the total amount of CRF mRNA in the PVN, as we did in the present study.…”

Section: Crf Neurons and Crfr1 And Crfr2 Imbalancementioning

confidence: 99%

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

et al. 2008

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Hyperactivity of corticotropin-releasing factor (CRF) neurons in the paraventricular nucleus (PVN) of the hypothalamus is a prominent feature in depression and may be important in the etiology of this disease. The activity of the CRF neurons in the stress response is modulated by a number of factors that stimulate or inhibit CRF expression, including (1) corticosteroid receptors and their chaperones, heat shock proteins 70 and 90, (2) sex hormone receptors, (3) CRF receptors 1 (CRFR1) and 2, (4) cytokines interleukin 1-b and tumor necrosis factor-a, (5) neuropeptides and receptors, vasopressin (AVP), AVP receptor 1a (AVPR1A) and oxytocin and (6) transcription factor cAMP-response element-binding protein. We hypothesized that, in depression, the transcript levels of those genes that are involved in the activation of the hypothalamo-pituitary-adrenal (HPA) axis are upregulated, whereas the transcript levels of the genes involved in the inhibition of the HPA axis are downregulated. We performed laser microdissection and real-time PCR in the PVN and as a control in the supraoptic nucleus. Snap-frozen post-mortem hypothalami of seven depressed and seven matched controls were used. We found significantly increased CRF mRNA levels in the PVN of the depressed patients. This was accompanied by a significantly increased expression of four genes that are involved in the activation of CRF neurons, that is, CRFR1, estrogen receptor-a, AVPR1A and mineralocorticoid receptor, while the expression of the androgen receptor mRNA involved in the inhibition of CRF neurons was decreased significantly. These findings raise the possibility that a disturbed balance in the production of receptors may contribute to the activation of the HPA axis in depression.

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Section: Crf Neurons and Crfr1 And Crfr2 Imbalancementioning

confidence: 99%

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

et al. 2008

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“…It is noteworthy that we have previously observed genetic associations (in the currently used trio data set) of common SNPs in neural conduction and neurotransmitter release (Wasserman et al, 2005), monoaminergic signaling (Wasserman et al, 2007;BenEfraim et al, 2012), and glutamatergic signaling genes . Interestingly, potential functional roles that are not directly related to mediating stress reactivity in depression and suicidal behavior have been shown for dysregulation of AVP (Merali et al, 2006;Mlynarik et al, 2007;Bao and Swaab 2010), but the role of AVPR1B genetics is still poorly understood.…”

Section: Avpr1b G â E Vs Genetic Associationsmentioning

confidence: 99%

Family-Based Study of AVPR1B Association and Interaction with Stressful Life Events on Depression and Anxiety in Suicide Attempts

Ben-Efraim

Wasserman

et al. 2013

Neuropsychopharmacol

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The cortisol response to psychosocial stress may become dysregulated in stress-related disorders. It is potentiated by pituitary secretion of adrenocorticotropic hormone (ACTH), which is, in part, regulated by arginine vasopressin receptor-1B (AVPR1B). AVPR1B variants were previously reported to associate with mood and anxiety disorders. This study aims, for the first time, to investigate association of AVPR1B genetic variants with mood and anxiety outcomes in suicidal behavior.Using a family-based study design of 660 complete nuclear family trios with offspring who have made a suicide attempt (SA), we tested the direct association and linkage of AVPR1B single nucleotide polymorphisms (SNPs) with SA, as well as with depression and anxiety in SA. Main findings were the association and linkage of AVPR1B exon 1 SNP rs33990840 and a major 6-SNP haplotype representative of all common AVPR1B-SNPs, on the outcome of high Beck Depression Inventory scores in SA. By contrast, genetic associations with lifetime diagnoses of depression and anxiety in SA or gene-environment interactions between AVPR1B variants and stressful life events (SLEs) were not significant. An exploratory screen of interactions between AVPR1B and CRHR1 (corticotropin-releasing hormone receptor-1), the principal pituitary regulator of ACTH secretion, showed no support for gene-gene interactions on the studied outcomes. The results suggest that AVPR1B genetic variation, eg, non-synonymous SNP rs33990840 mediating putative consequences on ligand binding, has a role in SA etiology characterized by elevated depression symptoms, without involving AVPR1B-moderation of SLEs.

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“…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).…”

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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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Corticotropin-Releasing Hormone, Arginine Vasopressin, Gastrin-Releasing Peptide, and Neuromedin B Alterations in Stress-Relevant Brain Regions of Suicides and Control Subjects

Cited by 140 publications

References 97 publications

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

Family-Based Study of AVPR1B Association and Interaction with Stressful Life Events on Depression and Anxiety in Suicide Attempts

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

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