In Vivo Corticotropin-Releasing Factor-Induced Secretion of Adrenocorticotropin, β-Endorphin, and Corticosterone*

Rivier, Catherine; Brownstein, M. J.; Spiess, Joachim; Rivier, Jean; Vale, Wylie

doi:10.1210/endo-110-1-272

Cited by 591 publications

(181 citation statements)

References 0 publications

Supporting

Mentioning

162

Contrasting

Unclassified

Order By: Relevance

“…Our finding of elevated basal ACTH levels 6-7 h after DEX pretreatment in male HAB rats, but not in male LAB rats, indicates a partial failure of DEX suppression in HAB rats. In male LAB rats subsequent CRH stimulation failed to induce an escape of ACTH and corticosterone from DEX suppression, which supports the idea of a reciprocal interaction between exogenous and/or endogenous glucocorticoid titers and the degree of pituitary-adrenocortical activation by CRH (Rivier et al 1982;Hatzinger et al 1996). In contrast, as in patients suffering from major depression (Holsboer and Barden 1996), male HAB rats responded with a substantial increase in ACTH and corticosterone.…”

supporting

confidence: 69%

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

supporting

confidence: 69%

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

show abstract

“…The corticotropin-releasing factor (CRF) system coordinates behavioral, neuroendocrine, and autonomic responses to stressors (Koob, 1999;Rivier et al, 1982). The CRF system might also be implicated in drug dependence.…”

Section: Introductionmentioning

confidence: 99%

CRF2 Receptor Deficiency Eliminates the Long-Lasting Vulnerability of Motivational States Induced by Opiate Withdrawal

Morisot

Rouibi

Contarino

2015

Neuropsychopharmacol

View full text Add to dashboard Cite

Vulnerability to stressful life events is a hallmark of drug dependence that may persist long after cessation of drug intake and dramatically fuel key clinical features, such as deregulated up-shifted motivational states and craving. However, to date, no effective therapy is available for reducing vulnerability to stressful events in former drug users and drug-dependent patients, mostly because of poor knowledge of the mechanisms underlying it. In this study, we report that genetic inactivation of the stress-responsive corticotropin-releasing factor receptor-2 (CRF 2 − / − ) completely eliminates the reemergence of increased nonrewarded nose-pokes, reflecting up-shifted motivational states, triggered by ethological environmental stressors long after cessation of morphine administration in mice. Accordingly, CRF 2 receptor deficiency completely abolishes the increase in biomarkers of synthesis of major brain motivational substrates, such as ventral tegmental area (VTA) dopamine (DA) and amygdala γ-aminobutyric acid (GABA) systems, associated with the stress-induced reemergence of upshifted motivational states long after opiate withdrawal. Nevertheless, neither CRF 2 receptor deficiency nor long-term opiate withdrawal affects amygdala CRF or hypothalamus CRF expression, indicating preserved brain stress-coping systems. Moreover, CRF 2 receptor deficiency does not influence the locomotor or the anxiety-like effect of long-term opiate withdrawal. Thus, the present results reveal an essential and specific role for the CRF 2 receptor in the stress-induced reemergence of up-shifted motivational states and related alterations in brain motivational systems long after opiate withdrawal. These findings suggest new strategies for the treatment of the severe and longlasting vulnerability that inexorably follows drug withdrawal and hinder drug abstinence.

show abstract

“…Corticotropin-releasing factor (CRF), a 41-amino acid peptide, has been isolated and characterized from extracts of ovine hypothalamus as a potent stimulator of the secretion of corticotropin (ACTH) and 3-endorphin (1)(2)(3). Immunocytochemical studies have established that most of the CRF in the hypothalamus is located both in neurons of the paraventricular nucleus and in terminals around portal capillaries of the median eminence (4)(5)(6)(7).…”

mentioning

confidence: 99%

Corticotropin-releasing factor (CRF)-like immunoreactivity in the vertebrate endocrine pancreas.

Petrusz¹,

Merchenthaler²,

Maderdrut³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The light microscopic immunocytochemical localization of corticotropin-releasing factor (CRF) is described in the endocrine pancreas of several species representing the major classes of vertebrates: fishes (channel catfish, Ictalurus punctatus), amphibians (African clawed toad, Xenopu8 laevis), reptiles (chameleon, Anolis carolinensis), birds (chicken, Gallus domesticus), and several mammals (rat, mouse, cat, rhesus monkey, and man). The CRF-containing cells are scattered over the entire islet tissue in primates and cat, whereas in rat and mouse they are located at the periphery of the islets. In the chicken and catfish, the CRF-containing cells are found in a central location within islets and form larger clusters or cords. Single cells with CRF-like immunoreactivity are interspersed between acinar cells of the exocrine pancreas in all species studied. The CRF cells show a substantial topographical overlap with glucagon cells, but their precise identity and function remain to be determined.Corticotropin-releasing factor (CRF), a 41-amino acid peptide, has been isolated and characterized from extracts of ovine hypothalamus as a potent stimulator of the secretion of corticotropin (ACTH) and 3-endorphin (1-3). Immunocytochemical studies have established that most of the CRF in the hypothalamus is located both in neurons of the paraventricular nucleus and in terminals around portal capillaries of the median eminence (4-7). CRF-like immunoreactivity has been identified in hypophysial portal blood (8). The neural pathways through which CRF reaches the median eminence also have been described (9). Like other neuropeptides, CRF is widely distributed in extrahypothalamic areas of the brain, determined by both radioimmunoassay (10) and immunocytochemistry (11)(12)(13). In addition to stimulating the release of ACTH and /8-endorphin, CRF has a broad range of pharmacological effects, which include changes in behavior, heart rate, blood pressure, and in blood concentrations of epinephrine, norepinephrine, glucagon, and glucose (14-18). Thus, CRF appears to be an important regulatory peptide mediating stress-related physiological responses and predictably possessing other, hitherto unsuspected, hormone-or neurotransmitter-like activities. On the basis of current hypotheses concerning the common evolutionary origin of hormones and neurotransmitters (19)(20)(21) (Altamont, NY). One African clawed toad (Xenopus laevis) and pancreatic tissue from two channel catfish (Ictalurus punctatus) were gifts from L. J. Haverkamp (Neurobiology Program, University of North Carolina) and J. E. Brinn (Department of Anatomy, East Carolina University), respectively. Three lizards (Anolis carolinensis) were purchased from Carolina Biological Supply (Burlington, NC). Pancreatic tissue from two adult cats and two adult rhesus monkeys (Macaca mulatta) also was studied. Human pancreas (courtesy of E. K. MacRae and F. D. Dalldorf) was from a 1-year-old infant who died in an accident.Preparation of Tissues. Rat, mouse, cat, monkey, chicken, ...

show abstract

In Vivo Corticotropin-Releasing Factor-Induced Secretion of Adrenocorticotropin, β-Endorphin, and Corticosterone*

Cited by 591 publications

References 0 publications

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

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

CRF2 Receptor Deficiency Eliminates the Long-Lasting Vulnerability of Motivational States Induced by Opiate Withdrawal

Corticotropin-releasing factor (CRF)-like immunoreactivity in the vertebrate endocrine pancreas.

Contact Info

Product

Resources

About