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The Journal of Neuroscience, November 5, 2008, 28(45):11583-11592; doi:10.1523/JNEUROSCI.2493-08.2008

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Behavioral/Systems/Cognitive
Cholecystokinin Regulates Expression of Y2 Receptors in Vagal Afferent Neurons Serving the Stomach

Galina Burdyga,¹ Guillaume de Lartigue,¹ Helen E. Raybould,³ Richard Morris,² Rod Dimaline,¹ Andrea Varro,¹ David G. Thompson,⁴ and Graham J. Dockray¹

¹Physiological Laboratory, School of Biomedical Sciences and ²School of Preclinical Veterinary Science, University of Liverpool, Liverpool L69 3BX, United Kingdom, ³Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis, Davis, California 95616, and ⁴Division of Gastroenterology, University of Manchester, Hope Hospital, Salford PR7 6JL, United Kingdom

Correspondence should be addressed to Graham J. Dockray, Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Crown Street, Liverpool L69 3BX, UK. Email: g.j.dockray{at}liverpool.ac.uk

The intestinal hormones CCK and PYY3–36 inhibit gastric emptying and food intake via vagal afferent neurons. Here we report that CCK regulates the expression of Y2R, at which PYY3–36 acts. In nodose ganglia from rats fasted up to 48 h, there was a fivefold decrease of Y2R mRNA compared with rats fed ad libitum; Y2R mRNA in fasted rats was increased by administration of CCK, and by refeeding through a mechanism sensitive to the CCK1R antagonist lorglumide. Antibodies to Y2R revealed expression in both neurons and satellite cells; most of the former (89 ± 4%) also expressed CCK1R. With fasting there was loss of Y2R immunoreactivity in CCK1R-expressing neurons many of which projected to the stomach, but not in satellite cells or neurons projecting to the ileum or proximal colon. Expression of a Y2R promoter-luciferase reporter (Y2R-luc) in cultured vagal afferent neurons was increased in response to CCK by 12.3 ± 0.1-fold and by phorbol ester (16.2 ± 0.4-fold); the response to both was abolished by the protein kinase C inhibitor Ro-32,0432. PYY3–36 stimulated CREB phosphorylation in rat nodose neurons after priming with CCK; in wild-type mice PYY3–36 increased Fos labeling in brainstem neurons but in mice null for CCK1R this response was abolished. Thus Y2R is expressed by functionally distinct subsets of nodose ganglion neurons projecting to the stomach and ileum/colon; in the former expression is dependent on stimulation by CCK, and there is evidence that PYY3–36 effects on vagal afferent neurons are CCK dependent.

Key words: satiety; Y2; PYY; CCK; ghrelin; vagus

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Received May 30, 2008; revised Sept. 22, 2008; accepted Sept. 27, 2008.

Correspondence should be addressed to Graham J. Dockray, Physiological Laboratory, School of Biomedical Sciences, University of Liverpool, Crown Street, Liverpool L69 3BX, UK. Email: g.j.dockray{at}liverpool.ac.uk

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