Vasopressin and ethanol preference. II. Altered preference in two strains of diabetes insipidus rats and nephrogenic diabetes insipidus mice

Crabbe, John C.; Rigter, Henk

doi:10.1016/0196-9781(85)90171-8

Cited by 10 publications

(2 citation statements)

References 13 publications

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“…Prolonged exposure to ethanol markedly decreases the number of Avp immunoreactive magnocellular neurons in the supraoptic nuclei and paraventricular nuclei (39). In addition, the role of Avp in ethanol preference and consumption has been studied in rats (13,18,36). Brattleboro strain rats, which lack vasopressin and have high fluid intakes, show reduced preference for ethanol and increased intake of ethanol (36).…”

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confidence: 99%

Alcohol preference in mice lacking the Avpr1a vasopressin receptor

Sanbe¹,

Takagi²,

Fujiwara³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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[Arg(8)]-vasopressin (Avp), a nonapeptide hormone, is known to regulate blood pressure, water balance, and a variety of behaviors such as anxiety, aggression, and bonding. Although some evidence that Avp modifies ethanol consumption and some of the effects of ethanol on behavior have been reported, the role of Avp in alcohol consumption and preference is poorly understood. The Avp1a receptor (Avpr1a) is ubiquitously expressed in the central nervous system. To determine the role of Avp signaling on the behavioral effects of alcohol, we examined voluntary ethanol consumption in mice with targeted disruptions of the Avpr1a knockout (Avpr1a KO) gene. Avpr1a KO mice displayed both increased ethanol consumption and preference compared with wild-type (WT) mice. Enhanced ethanol consumption was dramatically and reversibly reduced by treatment with N-methyl-D-aspartic acid antagonists. Basal glutamate release was elevated around the striatum in Avpr1a KO mice. Elevation of extracellular glutamate was also produced in WT mice by local application of an Avpr1a antagonist though a dialysis probe, and this elevation was quickly reversed by stopping the perfusion. These results suggest that Avp can inhibit the release of glutamate from the presynaptic terminal via the Avp1a receptor and that elevation of glutamate levels owing to loss of the inhibitory effect via Avp-Avpr1a signaling may play an important role in the preference for ethanol.

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mentioning

confidence: 99%

Alcohol preference in mice lacking the Avpr1a vasopressin receptor

Sanbe¹,

Takagi²,

Fujiwara³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Additionally, in rats, a reduction has been observed in the number of AVP immunoreactivity neurones and AVP mRNA levels in the hypothalamus region after chronic alcohol consumption . The role of AVP in ethanol preference and consumption was first described in Brattleboro rats by Crabbe and Rigter and Rigter and Crabbe They show that there is an increase in total fluid consumption, also increasing ethanol intake. Alcohol preference, however, was decreased.…”

Section: Alcohol and Vasopressinmentioning

confidence: 96%

Effects of alcohol and psychostimulants on the vasopressin system: Behavioural implications

Godino

Renard

2018

J Neuroendocrinology

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Drug addiction is a chronic brain disease characterized by a compulsion to seek drugs, a loss of control with respect to drug consumption, and negative emotional states, including increased anxiety and irritability during withdrawal. Central vasopressin (AVP) and its receptors are involved in controlling social behavior, anxiety and reward, all of which are altered by drugs of abuse. Hypothalamic AVP neurons influence the stress response by modulating the hypothalamic-pituitary-adrenal (HPA) axis. The extrahypothalamic AVP system, however, is commonly associated with social recognition, motivational and anxiety responses. The specific relationship between AVP and drugs of abuse has been rarely reviewed. Here, we provide an overview of the interaction between the brain AVP system and psychostimulants and alcohol. We focus on the effects of alcohol and psychostimulants on AVP regulation of the HPA axis, their effect on the brain AVP system and their behavioral implications, the influence of the AVP system on addictive behaviors, AVP's organizational effects on the brain and consequently on behavior, and we highlight clinical studies on the relation between the AVP system and drug addiction. Finally, we discuss the data to address areas that need further research to support clinical trials and prevent drug-related disorders. This article is protected by copyright. All rights reserved.

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Genetic Models of Diabetes Insipidus

Valtin

1992

Comprehensive Physiology

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The sections in this article are: Classification of Diabetes Insipidus Hypothalamic Diabetes Insipidus History of the Brattleboro Rat Biosynthesis of Vasopressin Pathophysiology of Hypothalamic Diabetes Insipidus Nephrogenic Diabetes Insipidus Description of Mouse Strains Causes: Corticopapillary Gradient vs. Water Permeability Defects in the Mouse Strains Pathophysiology of Nephrogenic Diabetes Insipidus Other Applications of the Models Amount of Water Reabsorbed from Collecting Ducts The Running Start Hyponatremia during Sodium Depletion Essentiality of Vasopressin Use of Both Models Simultaneously Nephron Heterogeneity Innervation of Vasopressin Neurons Alcohol Preference Summary and Concluding Remarks

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Vasopressin and ethanol preference. II. Altered preference in two strains of diabetes insipidus rats and nephrogenic diabetes insipidus mice

Cited by 10 publications

References 13 publications

Alcohol preference in mice lacking the Avpr1a vasopressin receptor

Alcohol preference in mice lacking the Avpr1a vasopressin receptor

Effects of alcohol and psychostimulants on the vasopressin system: Behavioural implications

Genetic Models of Diabetes Insipidus

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