Congenital vasopressin deficiency and acute and chronic opiate effects on hypothalamo-pituitary–adrenal axis activity in Brattleboro rats

Domokos, Ágnes; Mergl, Zsuzsa; Barna, István; Makara, Gábor B.; Zelena, Dóra

doi:10.1677/joe-07-0356

Cited by 18 publications

(17 citation statements)

References 33 publications

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“…By contrast, the application of similar stressors for only 2 weeks (i.e. repeated restraint (Zelena et al 2003), streptozotocin-induced diabetes mellitus (Zelena et al 2006), and repeated morphine withdrawal (Domokos et al 2008)) failed to reveal significant differences between the Brattleboro and control rats, indicating that AVP did not essentially contribute to the state of the HPA axis at this time point.…”

Section: Introductionmentioning

confidence: 80%

Blunted HPA axis response in lactating, vasopressin-deficient Brattleboro rats

Fodor¹,

Pintér²,

Domokos³

et al. 2013

Journal of Endocrinology

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Adaptation to stress is a basic phenomenon in mammalian life that is mandatorily associated with the activity of the hypothalamic-pituitary-adrenal (HPA) axis. An increased resting activity of the HPA axis can be measured during pregnancy and lactation, suggesting that these reproductive states lead to chronic load in females. In this study, we examined the consequences of the congenital lack of vasopressin on the activity of the HPA axis during lactation using vasopressindeficient Brattleboro rats. Virgin and lactating, homozygous vasopressin-deficient rats were compared with control, heterozygous rats. In control dams compared with virgins, physiological changes similar to those observed in a chronic stress state (thymus involution, adrenal gland hyperplasia, elevation of proopiomelanocortin mRNA levels in the adenohypophysis, and resting plasma corticosterone levels) were observed. In vasopressin-deficient dams, adrenal gland hyperplasia and resting corticosterone level elevations were not observed. Corticotropinreleasing hormone (Crh) mRNA levels in the hypothalamic paraventricular nucleus were elevated in only the control dams, while oxytocin (OT) mRNA levels were higher in vasopressin-deficient virgins and lactation induced a further increase in both the genotypes. Suckling-induced ACTH and corticosterone level elevations were blunted in vasopressin-deficient dams. Anaphylactoid reaction (i.v. egg white) and insulin-induced hypoglycemia stimulated the HPA axis, which were blunted in lactating rats compared with the virgins and in vasopressin-deficient rats compared with the controls without interaction of the two factors. Vasopressin seems to contribute to the physiological changes observed during lactation mimicking a chronic stress state, but its role in acute HPA axis regulation during lactation seems to be similar to that observed in virgins. If vasopressin is congenitally absent, OT, but not the CRH, compensates for the missing vasopressin; however, the functional restitution remains incomplete.

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Section: Introductionmentioning

confidence: 80%

Blunted HPA axis response in lactating, vasopressin-deficient Brattleboro rats

Fodor¹,

Pintér²,

Domokos³

et al. 2013

Journal of Endocrinology

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“…The plasma concentration of AVP, but not of OT, was significantly elevated in CRH-R1 KO mice, which is believed to be a compensatory mechanism to maintain basal ACTH secretion and HPA system activity under the CRH/CRH-R1 signal-deficient condition (356). Previous studies reported reduced basal ACTH and/or corticosterone levels in Brattleboro rats (74), whereas others reported no significant change of these parameters in Brattleboro rats (126,343,548). In V1bR-KO mice, only corticosterone was studied and was not decreased (533).…”

Section: The Hypothalamic-pituitary-adrenal Axismentioning

confidence: 86%

“…Morphine administration in Brattleboro rats produced a small yet significant reduction in the elevations of both ACTH and corticosterone levels (126). After repeated administration of morphine, ACTH levels of control rats were significantly elevated 16 h after the last morphine injection, with a smaller rise in Brattleboro rats (126). The intravenous administration of N-methyl-D-aspartate (NMDA, 5 mg/kg) or kainate (2.5 mg/kg) elevated the ACTH and corticosterone levels at 5 min in controls, but not in Brattleboro rats (552).…”

Section: The Hypothalamic-pituitary-adrenal Axismentioning

confidence: 93%

“…In rats, the acute administration of chemicals such as morphine and excitatory amino acids activates the HPA axis (69,76,552). Morphine administration in Brattleboro rats produced a small yet significant reduction in the elevations of both ACTH and corticosterone levels (126). After repeated administration of morphine, ACTH levels of control rats were significantly elevated 16 h after the last morphine injection, with a smaller rise in Brattleboro rats (126).…”

Section: The Hypothalamic-pituitary-adrenal Axismentioning

confidence: 99%

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Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

314

297

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The neurohypophysial hormone arginine vasopressin (AVP) is essential for a wide range of physiological functions, including water reabsorption, cardiovascular homeostasis, hormone secretion, and social behavior. These and other actions of AVP are mediated by at least three distinct receptor subtypes: V1a, V1b, and V2. Although the antidiuretic action of AVP and V2 receptor in renal distal tubules and collecting ducts is relatively well understood, recent years have seen an increasing understanding of the physiological roles of V1a and V1b receptors. The V1a receptor is originally found in the vascular smooth muscle and the V1b receptor in the anterior pituitary. Deletion of V1a or V1b receptor genes in mice revealed that the contributions of these receptors extend far beyond cardiovascular or hormone-secreting functions. Together with extensively developed pharmacological tools, genetically altered rodent models have advanced the understanding of a variety of AVP systems. Our report reviews the findings in this important field by covering a wide range of research, from the molecular physiology of V1a and V1b receptors to studies on whole animals, including gene knockout/knockdown studies.

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“…5c) (Zelena et al 2004. Subsequent studies, involving the application of other stressors in Brattleboro rats for two weeks (repeated morphine withdrawal: Domokos et al 2008; streptozotocininduced diabetes mellitus: Zelena et al 2006) also failed to reveal a clear impact of the lack of AVP on the (endocrine) chronic stress response. This may imply congenitally a, b and d) and corticosterone levels (c) in Brattleboro rats.…”

Section: Alterations Of Hpa Axis Regulation In Brattleboro Ratsmentioning

confidence: 99%

Vasopressin signaling at brain level controls stress hormone release: the vasopressin-deficient Brattleboro rat as a model

et al. 2015

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The nonapeptide arginine vasopressin (AVP) has long been suggested to play an important role as a secretagogue for triggering the activity of the endocrine stress response. Most recent studies employed mutant mice for analyzing the importance of AVP for endocrine regulation under stress. However, it is difficult to compare and draw overall conclusions from all these studies as mixing the genetic material from different mouse strains has consequences on the individual's stress response. Moreover, mice are not ideal subjects for several experimental procedures. Therefore, to get more insight, we used a rather old mutant rat model: the AVP-deficient Brattleboro rat. The present short review is aimed at providing the most interesting results of these studies within the last 8 years that allowed gaining new insights in the potential signal function of AVP in stress and endocrine regulation.

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Congenital vasopressin deficiency and acute and chronic opiate effects on hypothalamo-pituitary–adrenal axis activity in Brattleboro rats

Cited by 18 publications

References 33 publications

Blunted HPA axis response in lactating, vasopressin-deficient Brattleboro rats

Blunted HPA axis response in lactating, vasopressin-deficient Brattleboro rats

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Vasopressin signaling at brain level controls stress hormone release: the vasopressin-deficient Brattleboro rat as a model

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