Corticotropin releasing activity of the new CRF is potentiated several times by vasopressin

Gillies, Glenda; Linton, Elizabeth A.; Lowry, P. J.

doi:10.1038/299355a0

Cited by 979 publications

(435 citation statements)

References 17 publications

Supporting

Mentioning

411

Contrasting

Unclassified

Order By: Relevance

“…In addition, AVP released from the SON may induce ACTH release from the pituitary [59] . 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%

Section: Stimulatory Activity Of Crh and Avpmentioning

confidence: 99%

“…Some CRH neurons in the PVN co-express and release AVP. When released together into the hypophyseal-portal system, AVP strongly potentiates the ACTH-releasing activity of corticotrophs [59,60] .In addition, AVP released from the SON may induce ACTH release from the pituitary [59] . CRH and AVP stimulate ACTH secretion from pituitary corticotrophs by interacting with the CRH type 1 (CRHR1) and Avpr1b or V1b receptors, respectively [62] .…”

mentioning

confidence: 99%

See 2 more Smart Citations

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

View full text Add to dashboard Cite

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 ...

show abstract

Section: Stimulatory Activity Of Crh and Avpmentioning

confidence: 99%

Section: Stimulatory Activity Of Crh and Avpmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

View full text Add to dashboard Cite

show abstract

“…After the discovery of CRH (Vale et al 1981) it was rapidly established that AVP potently synergizes with CRH to stimulate pituitary ACTH secretion: when CRH and AVP are co-administered, hormone output is well above the combined effects of the two neuropeptides in both humans (von Bardeleben and Holsboer 1985) and rodents (Gillies et al 1982). AVP is mainly synthesized in the magnocellular neurons of the hypothalamic PVN and the supraoptic nucleus.…”

Section: Hyperactivity Of the Intra-pvn Vasopressinergic System: Majomentioning

confidence: 99%

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

Keck

Wigger

Welt

et al. 2002

Neuropsychopharmacology

157

View full text Add to dashboard Cite

To investigate the neuroendocrine alterations linked to inborn emotionality in two Wistar rat lines selectively bred for either high (HAB) or low (LAB) anxiety-related behavior, we administered the combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH)testNeuroendocrine studies provide strong indications that hyperactivity of central corticotropin-releasing hormone (CRH) circuits, resulting in a characteristic dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) system, plays a causal role in the symptomatology of affective and anxiety disorders (review: Keck and Holsboer 2001). The effects of CRH are modulated by vasopressin (AVP), which, after prolonged stress and in senescence, is increasingly coexpressed and secreted from hypothalamic CRH neurons in both humans and rodents (Antoni 1993;Tilders et al. 1993;Hatzinger et al. 2000;Keck et al. 2000). Similarly, increased numbers of CRH neurons that coexpress AVP mRNA have been found in the hypothalamus of depressed patients (Raadsheer et al. 1993;Purba et al. 1996). The excessive release of CRH and AVP into hypophysial portal blood is thought to increase the secretion of corticotropin (ACTH) from pituitary corticotrope cells, and this in turn to increase the release of corticosteroids from the adrenal gland. In this context, a variety of changes in HPA system regulation have been demonstrated in psychiatric disorders such as major depression, among them defective negative feedback of the HPA system, basal hypercortisolemia, inappropriate HPA suppression by the synthetic corticosteroid dexamethasone (DEX) and a paradoxical stimulation of ACTH secretion by CRH after DEX pretreatment (review: Holsboer and Barden 1996;Holsboer 2000). In depression, the combined DEX/CRH test, in which DEX-pretreated subjects receive a single dose of CRH, has proven to be the most sensitive tool for the detection of altered HPA regulation. Depending on age and gender, up to 90% of patients with depression show this neuroendocrine phenomenon (Heuser et al. 1994). Moreover, studies using the DEX/CRH test not only agree that normalization of an initial aberrance is predictive of a favorable treatment response but also corroborate other evidence that a persistent HPA abnormality correlates with chronicity or relapse (Heuser et al. 1996;Zobel et al. 1999). Since activation of corticosteroid receptors suppresses the synthesis and release of CRH and AVP from the hypothalamic paraventricular nucleus (PVN) , these findings are consistent with the hypothesis of functionally impaired corticosteroid receptor signaling in both depressed patients (Modell et al. 1997) and healthy subjects at genetic risk for depression Modell et al. 1998).As the mechanisms underlying the abnormal HPA reactivity in patients with certain psychiatric disorders are not fully understood, animal models are needed to further investigate the hypothesized linkage between these disorders and changes in the regulation of the HPA system. After several generations of selective breeding, we could establish ...

show abstract

“…CRF is synthesized and secreted in the hypothalamic paraventricular nucleus (PVN) in response to stress, and subsequently stimulates adrenocorticotropic hormone (ACTH), which is encoded by the pro-opiomelanocortin (POMC) gene in pituitary corticotrophs (Gillies et al, 1982;Mouri et l., 1993). ACTH stimulates the release of glucocorticoids from the adrenal glands, and these glucocorticoids play a variety of roles in the target tissues (Whitnall, 1993).…”

Section: It Is Well Known That Ultraviolet Radiation (Uvr) Stimulatesmentioning

confidence: 99%

Involvement of Nurr-1/Nur77 in corticotropin-releasing factor/urocortin1-induced tyrosinase-related protein 1 gene transcription in human melanoma HMV-II cells

Watanuki

Takayasu

Kageyama

et al. 2013

Molecular and Cellular Endocrinology

View full text Add to dashboard Cite

Corticotropin releasing activity of the new CRF is potentiated several times by vasopressin

Cited by 979 publications

References 17 publications

Hypothalamic-pituitary-adrenal axis function during perinatal depression

Hypothalamic-pituitary-adrenal axis function during perinatal depression

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

Involvement of Nurr-1/Nur77 in corticotropin-releasing factor/urocortin1-induced tyrosinase-related protein 1 gene transcription in human melanoma HMV-II cells

Contact Info

Product

Resources

About