Corticotropin Releasing Factor (CRF) Binding Protein: A Novel Regulator of CRF and Related Peptides

Behan, Dominic P.; Souza, Errol B. De; Lowry, P. J.; Potter, Ellen; Sawchenko, Paul E.; Vale, Wylie

doi:10.1006/frne.1995.1013

Cited by 225 publications

(157 citation statements)

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“…In the brain, CRH also binds to a protein, the CRH-binding protein (CRH-BP), which has the ability to inactivate CRH. 21 In recent years, a new peptide has been identi®ed in the rat brain and termed urocortin (UCN) 22 because of its homology for urotensin I and CRH. This 40 amino acid peptide is found in the Edinger ± Westphal nucleus, the supraoptic nucleus and the lateral hypothalamus.…”

Section: Crh Crh Receptors and Urocortinmentioning

confidence: 99%

The corticotropin-releasing hormone system in the regulation of energy balance in obesity

2000

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The view that energy balance is regulated has gained acceptance in recent years. An important role in this regulation is played by brain circuitries involved in the control of energy intake (food intake) and energy expenditure (thermogenesis) that are capable of integrating peripheral signals, produced by perturbations of adipose tissue mass, into messages to effectors of food intake and energy expenditure, so as to prevent substantial variations in the level of energy reserves. More than one neurosystem has been reported to genuinely participate in the regulation of energy balance. Among them is the corticotropin-releasing hormone (CRH) system. This system, with its numerous clusters of brain neurons, its closely related peptide urocortin, its two receptor types and its binding protein, all generally widely distributed throughout the brain, forms a network of neuronal pathways capable of interacting with the circuitries controlling food intake and energy expenditure. In addition, CRH and urocortin's anorectic and thermogenic actions appear to be coordinated to optimize energy losses. Finally, the CRH system seems to demonstrate a certain degree of plasticity in obesity and in response to food deprivation that is consistent with its action on food intake and thermogenesis. The observations have been made that food deprivation and obesity can blunt the expression of the CRH type 2a a receptor in the ventromedial hypothalamic nucleus and can induce the expression of the CRH-binding protein (a CRH-inactivating protein) in brain areas involved in the anorectic and thermogenic actions of CRH.

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Section: Crh Crh Receptors and Urocortinmentioning

confidence: 99%

The corticotropin-releasing hormone system in the regulation of energy balance in obesity

2000

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“…The CRF receptors are G protein-linked seven transmembrane domain receptors that are positively coupled to adenylate cyclase as well as other second messenger systems (Chen et al, 1993;Perrin et al, 1995). The CRF-BP binds CRF with an affinity equal to or higher than that of the receptors, and is thought to buffer the action of CRF by preventing interaction with the receptor and possibly targeting the peptide for degradation (Behan et al, 1995). Interestingly, recent work suggests that when CRF is bound to CRF-BP, this complex may act as a cellular signaling molecule (Ungless et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Roseboom

Nanda

Bakshi

et al. 2007

Psychoneuroendocrinology

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SummaryBehavioral inhibition (BI) is an adaptive defensive response to threat; however, extreme BI is associated with anxiety-related psychopathology. When rats are exposed to a natural predator they display stress-and anxiety-related behavioral alterations and physiological activation. To develop a preclinical rodent model to study mechanisms underlying human BI and anxiety, we examined the extent to which ferret exposure elicits anxiety-related BI and HPA and amygdala activation of the CRF system. In the first experiment, BI and other behaviors were assessed in the presence or absence of a ferret. In the second experiment, ferret-induced corticosterone release and changes in brain cfos expression were assessed. In the final experiment, gene chip and quantitative real time-PCR analyses were performed on amygdala tissue from control and ferret-exposed rats. Ferret exposure increased BI and submissive posturing, as well as plasma corticosterone and the number of Fospositive cells in several brain regions including the amygdala. Gene expression analysis revealed increased amygdalar mRNA for CRF-binding protein, but not the CRF 1 receptor, CRF 2 receptor or CRF. In rodents, ferret exposure can be used to elicit anxiety-related BI, which is associated with HPA and amygdala activation. Since the amygdala and the CRF system have been implicated in adaptive and maladaptive anxiety responses in humans, these data support use of our rodent model to further investigate mechanisms underlying anxiety-related psychopathology in humans.

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“…Ucn 2 is B1000-fold more CRF 2 -selective than Ucn 1, and Ucn 3 does not activate CRF 1 receptors Reyes et al, 2001;Hoare et al, 2005). Ucn 3 is unique in that it does not bind to the rat CRF-binding protein (Jahn et al, 2004), a secreted glycoprotein hypothesized to limit (Behan et al, 1995) or to allow (Ungless et al, 2003) CRF receptor agonist effects by complexing with ligand. Thus, Ucn 3 is a specific, direct CRF 2 receptor agonist.…”

Section: Introductionmentioning

confidence: 99%

Delayed Satiety-Like Actions and Altered Feeding Microstructure by a Selective Type 2 Corticotropin-Releasing Factor Agonist in Rats: Intra-Hypothalamic Urocortin 3 Administration Reduces Food Intake by Prolonging the Post-Meal Interval

Fekete

Inoue

Zhao

et al. 2006

Neuropsychopharmacol

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Brain corticotropin-releasing factor/urocortin (CRF/Ucn) systems are hypothesized to control feeding, with central administration of 'type 2' urocortins producing delayed anorexia. The present study sought to identify the receptor subtype, brain site, and behavioral mode of action through which Ucn 3 reduces nocturnal food intake in rats. Non-food-deprived male Wistar rats (n ¼ 176) were administered Ucn 3 into the lateral (LV) or fourth ventricle, or into the ventromedial or paraventricular nuclei of the hypothalamus (VMN, PVN) or the medial amygdala (MeA), regions in which Ucn 3 is expressed in proximity to CRF 2 receptors. LV Ucn 3 suppressed ingestion during the third-fourth post-injection hours. LV Ucn 3 anorexia was reversed by cotreatment with astressin 2 -B, a selective CRF 2 antagonist and not observed following equimole subcutaneous or fourth ventricle administration. Bilateral intra-VMN and intra-PVN infusion, more potently than LV infusion, reduced the quantity (57-73%) and duration of ingestion (32-68%) during the third-fourth post-infusion hours. LV, intra-PVN and intra-VMN infusion of Ucn 3 slowed the eating rate and reduced intake by prolonging the post-meal interval. Intra-VMN Ucn 3 reduced feeding bout size, and intra-PVN Ucn 3 reduced the regularity of eating from pellet to pellet. Ucn 3 effects were behaviorally specific, because minimal effective anorectic Ucn 3 doses did not alter drinking rate or promote a conditioned taste aversion, and site-specific, because intra-MeA Ucn 3 produced a nibbling pattern of more, but smaller meals without altering total intake. The results implicate the VMN and PVN of the hypothalamus as sites for Ucn 3-CRF 2 control of food intake.

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Corticotropin Releasing Factor (CRF) Binding Protein: A Novel Regulator of CRF and Related Peptides

Cited by 225 publications

References 0 publications

The corticotropin-releasing hormone system in the regulation of energy balance in obesity

The corticotropin-releasing hormone system in the regulation of energy balance in obesity

Predator threat induces behavioral inhibition, pituitary-adrenal activation and changes in amygdala CRF-binding protein gene expression

Delayed Satiety-Like Actions and Altered Feeding Microstructure by a Selective Type 2 Corticotropin-Releasing Factor Agonist in Rats: Intra-Hypothalamic Urocortin 3 Administration Reduces Food Intake by Prolonging the Post-Meal Interval

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