PT  - JOURNAL ARTICLE
AU  - Galina Burdyga
AU  - Simon Lal
AU  - Andrea Varro
AU  - Rod Dimaline
AU  - David G. Thompson
AU  - Graham J. Dockray
TI  - Expression of Cannabinoid CB1 Receptors by Vagal Afferent Neurons Is Inhibited by Cholecystokinin
AID  - 10.1523/JNEUROSCI.5404-03.2004
DP  - 2004 Mar 17
TA  - The Journal of Neuroscience
PG  - 2708--2715
VI  - 24
IP  - 11
4099  - http://www.jneurosci.org/content/24/11/2708.short
4100  - http://www.jneurosci.org/content/24/11/2708.full
SO  - J. Neurosci.2004 Mar 17; 24
AB  - 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.