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The Involvement of the Vasopressin System in Stress-Related Disorders
Abstract
The neuropeptide arginine vasopressin (AVP) is released within distinct brain areas upon appropriate stimulation, including stressful challenges. Following its predominantly dendritic release, AVP triggers a variety of receptor-mediated effects related to behavioral and neuroendocrine regulation. Antagonist treatment together with other sophisticated loss-of-function and gain-of-function approaches provide evidence for a multiple involvement of V1a and V1b receptor subtypes in stress-related behavior and disorders, including anxiety disorders, comorbid depression and their neuroendocrine concomitants. Conversely, in the high versus low anxiety (HAB/LAB) rat model, the phenotype of extreme trait anxiety is associated with a polymorphism-driven overexpression of AVP in the hypothalamic paraventricular nucleus. This overexpression of AVP might be considered a final common pathway of anxiety-related behavior. The capability of both responding to stressful stimuli and mediating genetic polymorphisms makes the central release of AVP a key process for converging (i.e., environmentally and genetically driven) behavioral regulation. Polymorphisms in the promoter structures of the AVP gene and AVP receptor genes, underlying differences in gene expression, thus contribute to individual variation in behavior as well as to psychopathology, making genes of the brain AVP system and their products a promising target for therapeutic interventions.
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“Its central actions are mediated by binding to the two G-protein coupled V 1A and V 1B receptors which are distributed in many anxiety-and fear-related brain areas including in the lateral septum, cortex and hippocampus, with V 1A receptors being the predominant receptor (Landgraf, 2006).”
From Novel pharmacological targets in drug development for the treatment of anxiety and anxiety-related disorders (2019) · cites this paper as Landgraf, 2006
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Neumann, I. D., & Landgraf, R. (2012) · Trends in Neurosciences · doi:10.1016/j.tins.2012.08.004 · Cited by 954
Self-citationThe prefrontal cortex as a key target of the maladaptive response to stress
Cerqueira, J. J., Mailliet, F., Almeida, O. F. X., Jay, T. M., & Sousa, N. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.4372-06.2007 · Cited by 599
“…AVP are peptides released as part of the stress response, that have receptors in several regions of the brain, including the hippocampus and the PFC (Szot et al., 1994; Herman et al., 2003); importantly, their release influences brain function and structure (Bayatti and Behl, 2005; Landgraf, 2006).”
BackgroundVasopressin: Behavioral roles of an “original” neuropeptide
Caldwell, H. K., Lee, H.-J., Macbeth, A. H., & Young, W. S. (2008) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2007.10.007 · Cited by 504
“HAB rats display greater depressive- and anxiety-like behaviors that are accompanied by enhanced stress-induced secretion of ACTH and corticosterone than LAB rats (Landgraf et al., 1999; Landgraf, 2006).”
BackgroundStress Hormone Regulation: Biological Role and Translation into Therapy
Holsboer, F., & Ising, M. (2010) · Annual Review of Psychology · doi:10.1146/annurev.psych.093008.100321 · Cited by 473
“Pretreatment by dexamethasone is indeed pertinent because opposite to cortisol, low dexamethasone dosages fail to cross the blood-brain barrier and result (on a functional level) in CNS hypocortisolism, which stimulates AVP (von Bardeleben & Holsboer 1989).”
BackgroundInfluentialSex differences in oxytocin and vasopressin: Implications for autism spectrum disorders?
CARTER, C. (2007) · Behavioural Brain Research · doi:10.1016/j.bbr.2006.08.025 · Cited by 432
“VP has been implicated in anxiety and in the stress-related upregulation of the HPA axis [112].”
Background
Metadata
- Authors
- Landgraf, R.
- Affiliations
- Max Planck Institute of Psychiatry (DE)
- Corresponding author
- Landgraf, Rainer
- Venue
- CNS & Neurological Disorders - Drug Targets
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2006-04-01
- Volume
- 5
- Issue
- 2
- Pages
- 167-179
- ISSN
- 1568-007X (ISSN-L)
- 1871-5273
- OpenAlex
- W2027012370
- Cited by
- 127
- References
- 0
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 6 · 2019: 1 · 2018: 3 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 7 · 2013: 6 · 2012: 8
- FWCI
- 22.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- CNS & Neurological Disorders - Drug Targets (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- vasopressin, vasopressin receptor, V1a receptor, V1b receptor, stress-related disorders, anxiety disorders, comorbid depression, hypothalamic paraventricular nucleus, trait anxiety, gene expression, neuroendocrine regulation, stress response, individual variation in behavior, therapeutic target
- MeSH terms
- Animals, Anxiety Disorders, Arginine Vasopressin, Gene Expression Regulation, Humans, Hypothalamo-Hypophyseal System, Paraventricular Hypothalamic Nucleus, Stress, Physiological, Receptors, Vasopressin, Mood Disorders, Genetic Predisposition to Disease
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