The role of vasopressin in diabetes mellitus-induced hypothalamo-pituitary-adrenal axis activation: Studies in Brattleboro rats

Zelena, Dóra; Mergl, Zsuzsa; Makara, Gábor B.

doi:10.1016/j.brainresbull.2005.10.009

Cited by 22 publications

(22 citation statements)

References 46 publications

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“…The unchanged somatic parameters (Table 2) as well as the retained corticosterone elevations did not support this assumption. The influence of peripheral AVP deficiency was excluded by using DDAVP containing osmotic minipumps (Zelena et al 2006b) thereby demonstrating that the changes observed in the present study were due to the loss of central vasopressinergic regulation.…”

Section: Discussionmentioning

confidence: 90%

“…Moreover, by cross-mating we have derived aC/C line from our original colony being in close relationship with each other (heterozygous breeding mothers are the daughters of the C/C mothers) and in one experiment (hypoglycaemia) we also used aC/C group as a control. To exclude the influence of peripheral AVP deficiency in one experiment (forced swim), an Alzet osmotic minipump (1 ml/h, 14 days) was implanted under the skin filled with 200 ml of 1 mg/ml desmopressine (DDAVP, V2 receptor agonist; Ferring Lieciva) under ether anaesthesia (Zelena et al 2006b). …”

Section: Animalsmentioning

confidence: 99%

“…Radiograms were evaluated by the ImageJ program (http://rsbweb.nih.gov/ij/). The integrated densities for the nucleus paraventricularis hypothalami (PVN) (Crh mRNA; Barna et al 2003, Zelena et al 2003a or the average densities for the hypophysis (Pomc mRNA; Zelena et al 2007) were calculated. The data were summarised from three hybridisation series expressing the levels of AVP-deficient animals as a percentage of their heterozygous littermate controls.…”

Section: In Situ Hybridisationmentioning

confidence: 99%

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The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

Zelena

Domokos

Jain

et al. 2009

Journal of Endocrinology

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Adaptation to a constantly changing environment is fundamental to every living organism. The hypothalamicpituitary-adrenocortical (HPA) axis is a key component of the adaptation process. The present study tests the hypothesis that vasopressin (AVP) is required for the HPA response to acute stimuli. To accomplish this, naturally AVP-deficient Brattleboro rats were exposed to a wide range of stimuli and their HPA response was compared with heterozygous littermattes. The circadian rhythmicity of plasma ACTH and corticosterone was not different between the two genotypes. The ACTH and corticosterone response to volume load, restraint or aggressive attack were decreased in AVP-deficient rats. The stress-induced increase in ACTH, but not corticosterone, was significantly impaired in AVPdeficient animals after novelty, elevated plus-maze, forced swim, hypoglycaemia, ulcerogenic cold immobilisation, lipopolysaccharide, hypertonic saline and egg white injection. The HPA response to social avoidance, ether inhalation and footshock was not different between the genotypes. In vitro, the hypophysis of AVP-deficient animals showed a reduction in stimulated ACTH production and their adrenal glands were hyporeactive to ACTH. A dissociation between the ACTH and corticosterone response was observed in several experiments and could not be explained by an earlier ACTH peak or enhanced adrenal sensitivity, suggesting the existence of paraadenohypophyseal neuroendocrine regulators. Loss of AVP affected the HPA response to a wide variety of stressors. Interestingly, the contribution of AVP to the HPA response was not specific for, nor limited to, a known stressor category. Thus, there is a context-specific requirement for AVP in stress-induced activation of the HPA axis.

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Section: Discussionmentioning

confidence: 90%

Section: Animalsmentioning

confidence: 99%

Section: In Situ Hybridisationmentioning

confidence: 99%

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The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

Zelena

Domokos

Jain

et al. 2009

Journal of Endocrinology

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“…in the renal collecting duct, we used a chronic subcutaneous treatment with a V2-receptor agonist, desmopressin (DDAVP; 1-deamino-8-D-arginine vasopressin) to compensate the peripheral lack of AVP (Robinson, 1976, Bankir, 2001, Makaryus and McFarlane, 2006. To analyse behavioral consequences of this treatment we used a battery of different tests primarily aimed at investigating emotional behavior and learning and memory that have not previously been applied in similar studies using Brattleboro rats and DDAVP treatment (Zelena et al, 2006, Feifel et al, 2007. Anxietyrelated behavior was studied by EPM, marble burying test (MB), defensive withdrawal (DW) and anhedonia was detected by sucrose preference (Misslin and Cigrand, 1986).…”

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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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“…However, the inhibitory action of a single injection of several oxytocin antagonists (Johnston & Negro-Vilar 1988) as well as of atosiban (Wilson 2007) was not supported by the results reported by other authors. The action of atosiban on prolactin release does not seem to be mediated by the blockade of vasopressin receptors, as prolactin concentrations were unchanged in vasopressin-deficient Brattleboro rats (Zelena et al 2006).…”

Section: Discussionmentioning

confidence: 88%

Effects of atosiban on stress-related neuroendocrine factors

Babic¹,

Pokusa²,

Danevova³

et al. 2015

Journal of Endocrinology

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Atosiban, an oxytocin/vasopressin receptor antagonist, is used to decrease preterm uterine activity. The risk of preterm delivery is undoubtedly associated with stress, but potential side effects of atosiban on neuroendocrine functions and stress-related pathways are mostly unknown. These studies were designed to test the hypothesis that the chronic treatment of rats with atosiban modulates neuroendocrine functions under stress conditions. Male rats were treated (osmotic minipumps) with atosiban (600 mg/kg per day) or vehicle and were restrained for 120 min/day for 14 days. All animals were treated with a marker of cell proliferation 5-bromo-2-deoxyuridine. Anxiety-like behavior was measured using an elevated plus-maze. Treatment with atosiban failed to modify plasma concentrations of the stress hormones ACTH and corticosterone, but led to a rise in circulating copeptin. Atosiban increased prolactin levels in the non-stressed group. Oxytocin receptor mRNA levels were increased in rats exposed to stress. Treatment with atosiban, in both control and stressed animals, resulted in a decrease in oxytocin receptor gene expression in the hypothalamus. No changes were observed in vasopressin receptor 1A and 1B gene expression. The decrease in hippocampal cell proliferation induced by stress exposure was not modified by atosiban treatment. This study provides the first data, to our knowledge, revealing the effect of atosiban on gene expression of oxytocin receptors in the brain. Atosiban-induced enhancement of plasma copeptin indicates an elevation in vasopressinergic tone with potential influence on water-electrolyte balance.

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The role of vasopressin in diabetes mellitus-induced hypothalamo-pituitary-adrenal axis activation: Studies in Brattleboro rats

Cited by 22 publications

References 46 publications

The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

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

Effects of atosiban on stress-related neuroendocrine factors

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