The Hypothalamic-Pituitary-Adrenal Axis Response to Stress in Mice Lacking Functional Vasopressin V1b Receptors

Lolait, Stephen J.; Stewart, Lesley Q.; Jessop, David S.; Young, rd W. Scott; O’Carroll, Anne-Marie

doi:10.1210/en.2006-1309

Cited by 132 publications

(126 citation statements)

References 78 publications

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“…It is noteworthy that in contrast to rats (Aguilera, 1998;Maet al, 1999), wild type mice shoved no habituation of ACTH responses to the repeated homotypic stress of restraint. However, V1b receptor knock out mice showed no responses to restraint stress on day 14, suggesting that V1b receptors are required for sustained responses to repeated stress (Lolait et al, 2007a). Although ACTH responses are reduced, these mice are able to display sustained corticosterone responses to the repeated stimuli.…”

Section: Does Vp Mediate Acth Responsiveness During Chronic Stress?mentioning

confidence: 98%

“…On the other hand, studies in V1b receptor knockout mice show clear compromise of HPA axis responses to some stressors. Studies using a mouse carrying a deletion of the 3' end of the coding region of the V1b receptor show reduced ACTH responses to acute hypoglycemia, lipopolysaccharide and ethanol administration but normal basal and acute restraint-stimulated ACTH (Lolait et al, 2007a;Lolait et al, 2007b;Tanoue et al, 2004;Wersinger et al, 2002). It is noteworthy that in contrast to rats (Aguilera, 1998;Maet al, 1999), wild type mice shoved no habituation of ACTH responses to the repeated homotypic stress of restraint.…”

Section: Does Vp Mediate Acth Responsiveness During Chronic Stress?mentioning

confidence: 99%

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The parvocellular vasopressinergic system and responsiveness of the hypothalamic pituitary adrenal axis during chronic stress

Aguilera

Subburaju

Young

et al. 2008

Progress in Brain Research

132

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Vasopressin (VP) secreted from parvocellular neurons of the hypothalamic paraventricular nucleus (PVN) stimulates pituitary ACTH secretion, through interaction with receptors of the V1b subtype (V1bR) in the pituitary corticotroph, mainly by potentiating the stimulatory effects of corticotrophin releasing hormone (CRH). Chronic stress paradigms associated with corticotroph hyperresponsiveness lead to preferential expression of hypothalamic VP over CRH and upregulation of pituitary V1bR, suggesting that VP has a primary role during adaptation of the hypothalamic pituitary adrenal (HPA) axis to long-term stimulation. However, studies using pharmacological of genetic ablation of V1b receptors have shown that VP is required for full ACTH responses to some stressors, but not for the sensitization of ACTH responses to a novel stress observed during chronic stress. Studies using minipump infusion of a peptide V1 antagonist in long-term adrenalectomized rats have revealed that VP mediates proliferative responses in the pituitary. Nevertheless, only a minor proportion of cells undergoing mitogenesis co-express markers for differentiated corticotrophs or precursors, suggesting that new corticotrophs are recruited from yet undifferentiated cells. The overall evidence supports a limited role of VP regulating acute ACTH responses to some acute stressors and points to cell proliferation and pituitary remodeling as alternative roles for the marked increases in parvocellular vasopressinergic activity during prolonged activation of the HPA axis.

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Section: Does Vp Mediate Acth Responsiveness During Chronic Stress?mentioning

confidence: 98%

Section: Does Vp Mediate Acth Responsiveness During Chronic Stress?mentioning

confidence: 99%

The parvocellular vasopressinergic system and responsiveness of the hypothalamic pituitary adrenal axis during chronic stress

Aguilera

Subburaju

Young

et al. 2008

Progress in Brain Research

132

View full text Add to dashboard Cite

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“…CRH and AVP stimulate ACTH secretion from pituitary corticotrophs by interacting with the CRH type 1 (CRHR1) and Avpr1b or V1b receptors, respectively [62] .…”

Section: Stimulatory Activity Of Crh and Avpmentioning

confidence: 99%

“…In contrast, AVP responses mediated through the Avpr1b receptor subtype activate the phospholipase C signaling system [57,66] . The Avpr1b receptor signaling system is required for normal pituitary and adrenal responses to acute stressful stimuli and is crucial for the ACTH-release response to chronic stressors [62,66] . Moreover, previous studies have shown that AVP responses to chronic stress are stimulated by GCs, which enhance the expression of Avpr1b receptor mRNA in the hypothalamus.…”

Section: Crh/avp Receptor Signaling Systemsmentioning

confidence: 99%

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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Abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis is an important pathological finding in pregnant women exhibiting major depressive disorder. They show high levels of cortisol proinflammatory cytokines, hypothalamic-pituitary peptide hormones and catecholamines, along with low dehydroepiandrosterone levels in plasma. During pregnancy, the TH2 balance together with the immune system and placental factors play crucial roles in the development of the fetal allograft to full term. These factors, when altered, may generate a persistent dysfunction of the HPA axis that may lead to an overt transfer of cortisol and toxicity to the fetus at the expense of reduced activity of placental 11β-hydroxysteroid dehydrogenase type 2. Epigenetic modifications also may contribute to the dysregulation of the HPA axis. Affective disorders in pregnant women should be taken seriously, and therapies focused on preventing the deleterious effects of stressors should be implemented to promote the welfare of both mother and baby.Keywords: brain; depression; neuroendocrine; pregnancy; stress; glucocorticoids Extensive studies have demonstrated that early life stressors produce changes in behavior and enhance the sensitivity of the stress response systems [1][2][3][4] . Although the genetic background has been implicated in the development of mood-related disorders, and genetic research has identified some chromosomal regions and genes that are involved in susceptibility to mood disorders, the etiology of anxiety and depressive disorders is still not clear in humans, particularly in women with major depressive disorder (MDD) [1] .The pathogenesis of perinatal depression is an emerging field. Although considerable progress has been made in this area in the last few years, there still remain unanswered questions and gaps in our knowledge of the underlying pathogenesis, the long-term impact of perinatal depression on the developing fetus, and the best methods for counseling pregnant women concerning the risks of untreated MDD versus the risks of psychopharmacologic treatment during pregnancy and lactation [5] . Meta-analysis studies have reported that the mean prevalence rate of prenatal depression is ~12% (this varies greatly according to location, mode of assessment, and socioeconomic conditions), and show that a large percentage of pregnant women displaying major depression remain depressed in the postpartum period and/or continuously [6,7] . Anxiety, depressive disorder, and stress during pregnancy are risk Phillipe Leff Gelman, et al. HPA axis in perinatal depression 339 factors for negative outcomes in newborns, like preterm birth or low birth weight; also, insecure attachment and impaired child development could be a consequence of mental disorders during pregnancy [6,[8][9][10] . The mechanisms by which maternal depression impacts fetal and neonatal development are currently under investigation; there is some evidence that depressive symptoms impact the infant's hypothalamic-pituitary-adrenal (HPA) axis, enhancing the ...

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“…Whereas the effects on the HPA axis are mediated by AVP/V 3 signaling in the hypothalamus (11,16,30), behavioral, and possibly autonomic, responses to stress are mediated by extrahypothalamic AVP/V 3 signaling in limbic structures, including the amygdala, hippocampus, and lateral septum (25,52). Although in acute stress responses CRF is the main activator of ACTH secretion, the AVP/V 3 system seems to play a major role during the adaptation to chronic stress conditions (1,19,26). During chronic stress, it has been shown that the hypothalamic content of AVP and V 3 receptor expression in the brain increases (2) and the peptide becomes the main modulator of the HPA axis (1,13,15,19).…”

mentioning

confidence: 99%

Involvement of vasopressin 3 receptors in chronic psychological stress-induced visceral hyperalgesia in rats

Bradesi¹,

Martínez²,

Lao³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Bradesi S, Martinez V, Lao L, Larsson H, Mayer EA. Involvement of vasopressin 3 receptors in chronic psychological stressinduced visceral hyperalgesia in rats. Am J Physiol Gastrointest Liver Physiol 296: G302-G309, 2009. First published November 25, 2008 doi:10.1152/ajpgi.90557.2008.-Visceral hypersensitivity and stress have been implicated in the pathophysiology of functional gastrointestinal disorders. We used a selective vasopressin 3 (V 3) receptor antagonist SSR149415 to investigate the involvement of the vasopressin (AVP)/V 3 signaling system in the development of stress-induced visceral hyperalgesia in rats. Rats were exposed to a daily 1-h session of water avoidance stress (WAS) or sham WAS for 10 consecutive days. The visceromotor response to phasic colorectal distension (CRD, 10 -60 mmHg) was assessed before and after stress. Animals were treated daily with SSR149415 (0.3, 1, or 3 mg/kg ip 30 min before each WAS or sham WAS session), with a single dose of SSR149415 (1 mg/kg ip), or the selective corticotropin-releasing factor 1 (CRF 1) antagonist DMP-696 (30 mg/kg po) before CRD at day 11. Effects of a single dose of SSR149415 (10 mg/kg iv) on acute mechanical sensitization during repetitive CRD (12 distensions at 80 mmHg) were also assessed. In vehicle-treated rats, repeated WAS increased the response to CRD, indicating visceral hypersensitivity. Repeated administration of SSR149415 at 1 or 3 mg/kg completely prevented stress-induced visceral hyperalgesia. Similarly, a single dose of DMP-696 or SSR149415 completely blocked hyperalgesic responses during CRD. In contrast, a single dose of SSR149415 did not affect the acute hyperalgesic responses induced by repeated, noxious distension. These data support a major role for V 3 receptors in repeated psychological stress-induced visceral hyperalgesia and suggest that pharmacological manipulation of the AVP/V 3 pathway might represent an attractive alternative to the CRF/CRF 1 pathway for the treatment of chronic stress-related gastrointestinal disorders. corticotropin-releasing factor; DMP-696; functional gastrointestinal disorders; irritable bowel syndrome; SSR149415RECURRENT ABDOMINAL PAIN ASSOCIATED with altered bowel habits and increased perception of physiological and experimental colonic stimuli (visceral hypersensitivity) are characteristic findings in patients with irritable bowel syndrome (IBS) (4). Although the pathophysiological basis of IBS is incompletely understood, epidemiological and experimental data indicate an important role of altered brain-gut interactions in this disorder. For example, many studies have highlighted the importance of certain types of psychological stress in the onset, maintenance, and exacerbation of IBS symptoms (5, 6, 32, 33). Furthermore, higher levels of anxiety, symptom-related anxiety, and comorbidity with anxiety disorders or depression are common in patients with IBS (32,33,49). Recent brain imaging studies have shown greater activation of limbic and paralimbic brain regions (including the amygdala) in patient...

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The Hypothalamic-Pituitary-Adrenal Axis Response to Stress in Mice Lacking Functional Vasopressin V1b Receptors

Cited by 132 publications

References 78 publications

The parvocellular vasopressinergic system and responsiveness of the hypothalamic pituitary adrenal axis during chronic stress

The parvocellular vasopressinergic system and responsiveness of the hypothalamic pituitary adrenal axis during chronic stress

Hypothalamic-pituitary-adrenal axis function during perinatal depression

Involvement of vasopressin 3 receptors in chronic psychological stress-induced visceral hyperalgesia in rats

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