The cholecystokinin B receptor also known as CCKBR or CCK2 is a protein[5] that in humans is encoded by the CCKBR gene.[6]
CCKBR | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Aliases | CCKBR, CCK-B, CCK2R, GASR, cholecystokinin B receptor | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 118445 MGI: 99479 HomoloGene: 7258 GeneCards: CCKBR | ||||||||||||||||||||||||||||||||||||||||||||||||||
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This gene encodes a G protein-coupled receptor for gastrin and cholecystokinin (CCK),[7][8][9] regulatory peptides of the brain and gastrointestinal tract. This protein is a type B gastrin receptor, which has a high affinity for both sulfated and nonsulfated CCK analogs and is found principally in the central nervous system and the gastrointestinal tract. A misspliced transcript variant including an intron has been observed in cells from colorectal and pancreatic tumors.[10]
CCK receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B expression may correlate parallel to anxiety and depression phenotypes in humans. CCK-B receptors possess a complex regulation of dopamine activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the dopamine-enhancing effects of CCK-A. However, the effects of CCK-B on dopamine activity vary depending on location.[11] CCK-B antagonism enhances dopamine release in rat striatum.[12] Activation enhances GABA release in rat anterior nucleus accumbens.[13] CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.[14] CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.[15]
In rats, CCK-B antagonism prevents the stress-induced reactivation of cocaine-induced conditioned place preference, and prevents the long-term maintenance and reinstatement of morphine-induced CPP.[16] Blockade of CCK-B potentiates cocaine-induced dopamine overflow in rat striatum.[12] CCK-B may pose a modulatory role in parkinson's disease. Blockade of CCK-B in dopamine-depleted squirrel monkeys induces significant enhancement of locomotor response to L-DOPA.[17] One study shows that visual hallucinations in Parkinson's disease are associated with cholecystokinin −45C>T polymorphism, and this association is still observed in the presence of the cholecystokinin-A receptor TC/CC genotype, indicating a possible interaction of these two genes in the visual hallucinogenesis in Parkinson's disease.[18]
The cholecystokinin B receptor is stimulated by CCK and gastrin in the stomach during digestion.
The cholecystokinin B receptor responds to a number of ligands.
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: CS1 maint: DOI inactive as of March 2024 (link)This article incorporates text from the United States National Library of Medicine, which is in the public domain.