CCK-B receptor: chemistry, molecular biology, biochemistry and pharmacology

Noble, Florence; Roques, Bernárd P.

doi:10.1016/s0301-0082(98)00090-2

Cited by 156 publications

(127 citation statements)

References 250 publications

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“…Moreover, CCKBR-KO mice show enhanced water consumption compared to WT mice (Noble and Roques, 1999). Based on these studies, I speculated that CCK may be involved in the control of driving neurons for thirst in the SFO.…”

Section: Iv1 Introductionmentioning

confidence: 98%

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

et al. 2016

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Section: Iv1 Introductionmentioning

confidence: 98%

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

et al. 2016

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“…CCK 1 receptors appear to mediate the transmission of sensory information from the gut to the brain. CCK is released from the intestine after a meal and then activates CCK 1 receptors on the vagus nerve in order to transmit sensations of fullness to the brain which subsequently terminates feeding behaviours (Kurosawa et al 1997;Noble et al 1999;Sternini et al 1999) or GIT responses. Recently, the responses to intestinal lipids (chylomicron components) and proteins involving this neurohormonal pathway were documented in detail by Glatzle et al (2003) and Darcel et al (2005).…”

Section: Molecular Formsmentioning

confidence: 99%

“…The CCK 1 receptor binds to sulfated CCK at 500-to 1000-fold higher affinity than to gastrin, whereas the CCK 2 receptor interacts with gastrin and CCK with almost the same affinity (Jensen et al 1989). These two subtypes of receptors were previously called CCK-A and CCK-B (or CCK-B/gastrin), respectively, and they were renamed CCK 1 and CCK 2 receptors following the International Union of Pharmacology Committee on Receptor Nomenclature and Drug Classification (Vanhoutte et al 1996;Noble et al 1999). The main characteristics of these two major subtypes of CCK and gastrin receptors known until now have been well described along with the transduction mechanisms responsible for their message translation (Wank, 1995;Yassin, 1999;Fourmy et al 2002;Miyasaka & Funakoshi, 2003).…”

Section: Introductionmentioning

confidence: 99%

Gastrin, cholecystokinin and gastrointestinal tract functions in mammals

et al. 2006

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The aim of the present review is to synthesise and summarise our recent knowledge on the involvement of cholecystokinin (CCK) and gastrin peptides and their receptors in the control of digestive functions and more generally their role in the field of nutrition in mammals. First, we examined the release of these peptides from the gut, focusing on their molecular forms, the factors regulating their release and the signalling pathways mediating their effects. Second, general physiological effects of CCK and gastrin peptides are described with regard to their specific receptors and the role of CCK on vagal mucosal afferent nerve activities. Local effects of CCK and gastrin in the gut are also reported, including gut development, gastrointestinal motility and control of pancreatic functions through vagal afferent pathways, including NO. Third, some examples of the intervention of the CCK and gastrin peptides are exposed in diseases, taking into account intervention of the classical receptor subtypes (CCK 1 and CCK 2 receptors) and their heterodimerisation as well as CCK-C receptor subtype. Finally, applications and future challenges are suggested in the nutritional field (performances) and in therapy with regards to the molecular forms or in relation with the type of receptor as well as new techniques to be utilised in detection or in therapy of disease. In conclusion, the present review underlines recent developments in this field: CCK and gastrin peptides and their receptors are the key factor of nutritional aspects; a better understanding of the mechanisms involved may increase the efficiency of the nutritional functions and the treatment of abnormalities under pathological conditions.

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“…It has been proposed that the opioid receptor signaling pathway is adaptively regulated at the cellular level, although more recently a growing contribution of the plasticity of neuronal networks involving opioidergic neurons has been recognized. In support of this latter hypothesis, a number of neuropeptides, including cholecystokinin (CCK) 2 , neuropeptide FF (NPFF) 3 and nociceptin (orphanin FQ) 4 , have been proposed as modulators of the opioid system. These various peptidergic pathways are collectively designated as an anti-opioid system.…”

mentioning

confidence: 99%

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

et al. 2005

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Prolactin-releasing peptide (PrRP) and its receptor G protein-coupled receptor 10 (GPR10) are expressed in brain areas involved in the processing of nociceptive signals. We investigated the role of this new neuropeptidergic system in GPR10-knockout mice. These mice had higher nociceptive thresholds and stronger stress-induced analgesia than wild-type mice, differences that were suppressed by naloxone treatment. In addition, potentiation of morphine-induced antinociception and reduction of morphine tolerance were observed in mutants. Intracerebroventricular administration of PrRP in wild-type mice promoted hyperalgesia and reversed morphine-induced antinociception. PrRP administration had no effect on GPR10-mutant mice, showing that its effects are mediated by GPR10. Anti-opioid effects of neuropeptide FF were found to require a functional PrRP-GPR10 system. Finally, GPR10 deficiency enhanced the acquisition of morphine-induced conditioned place preference and decreased the severity of naloxone-precipitated morphine withdrawal syndrome. Altogether, our data identify the PrRP-GPR10 system as a new and potent negative modulator of the opioid system.Opiate drugs, the prototype of which is morphine, are used largely for the treatment of severe pain. However, the prolonged use of opiate drugs induces a behavioral adaptation that results in the development of tolerance and dependence 1 . Although these adaptive mechanisms have been known for decades, the underlying pathophysiological pathways have not been fully clarified. It has been proposed that the opioid receptor signaling pathway is adaptively regulated at the cellular level, although more recently a growing contribution of the plasticity of neuronal networks involving opioidergic neurons has been recognized. In support of this latter hypothesis, a number of neuropeptides, including cholecystokinin (CCK) 2 , neuropeptide FF (NPFF) 3 and nociceptin (orphanin FQ) 4 , have been proposed as modulators of the opioid system. These various peptidergic pathways are collectively designated as an anti-opioid system. However, the action of individual peptides on the opioid pathway and on the processing of nociceptive signals is complex and some aspects remain controversial, particularly as the behavioral consequences can vary depending on the injection site of these peptides and the precise experimental setup 5,6 . Among these peptides, NPFF, which belongs to the RF-amide peptide family, was shown (among other actions) to regulate blood pressure 7 , prolactin release 8 and nociceptive signal processing 9 . Prolactin-releasing peptide (PrRP) has recently been identified as an additional member of the mammalian RF-amide peptide family, following its isolation as the natural agonist of the previously orphan GPR10 (ref. 10) (also known as hGR3 in human or UHR-1 in rat). Intracerebroventricular (i.c.v.) administration of PrRP affects feeding behavior 11 , blood pressure 12 and neuroendocrine processes, such as corticotropin-releasing hormone (CRH) 13 and oxytocin 14 release.In a...

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CCK-B receptor: chemistry, molecular biology, biochemistry and pharmacology

Cited by 156 publications

References 250 publications

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

Gastrin, cholecystokinin and gastrointestinal tract functions in mammals

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

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