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The Journal of Neuroscience, March 17, 2004, 24(11):2708-2715; doi:10.1523/JNEUROSCI.5404-03.2004

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Behavioral/Systems/Cognitive
Expression of Cannabinoid CB1 Receptors by Vagal Afferent Neurons Is Inhibited by Cholecystokinin

Galina Burdyga,¹ Simon Lal,¹ Andrea Varro,¹ Rod Dimaline,¹ David G. Thompson,² and Graham J. Dockray¹

¹Physiological Laboratory, University of Liverpool, Liverpool L69 3BX, United Kingdom, and ²Division of Gastroenterology, Hope Hospital, University of Manchester, Manchester M6 8HD, United Kingdom

Both inhibitory (satiety) and stimulatory (orexigenic) factors from the gastrointestinal tract regulate food intake. In the case of the satiety hormone cholecystokinin (CCK), these effects are mediated via vagal afferent neurons. We now report that vagal afferent neurons expressing the CCK-1 receptor also express cannabinoid CB1 receptors. Retrograde tracing established that these neurons project to the stomach and duodenum. The expression of CB1 receptors determined by RT-PCR, immunohistochemistry and in situ hybridization in rat nodose ganglia was increased by withdrawal of food for 12 hr. After refeeding of fasted rats there was a rapid loss of CB1 receptor expression identified by immunohistochemistry and in situ hybridization. These effects were blocked by administration of the CCK-1 receptor antagonist lorglumide and mimicked by administration of CCK to fasted rats. Because CCK is a satiety factor that acts via the vagus nerve and CB1 agonists stimulate food intake, the data suggest a new mechanism modulating the effect on food intake of satiety signals from the gastrointestinal tract.

Key words: afferent; appetite; cannabinoids; CCK; cholecystokinin; satiety; vagus

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Received Dec 8, 2003; revised January 22, 2004; accepted January 23, 2004.

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