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Title: Evidence for an Interaction between CB₁ Cannabinoid and Melanocortin MCR-4 Receptors in Regulating Food Intake
Contributor(s): Verty, Aaron N (author); McFarlane, James Robert (author)orcid ; McGregor, Iain (author); Mallet, Paul Emile (author)
Publication Date: 2004
Open Access: Yes
DOI: 10.1210/en.2004-0059
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Abstract: Melanocortin receptor 4 (MCR4) and CB₁ cannabinoid receptors independently modulate food intake. Although an interaction between the cannabinoid and melanocortin systems has been found in recovery from hemorrhagic shock, the interaction between these systems in modulating food intake has not yet been examined. The present study had two primary purposes: 1) to examine whether the cannabinoid and melanocortin systems act independently or synergistically in suppressing food intake; and 2) to determine the relative position of the CB₁ receptors in the chain of control of food intake in relation to the melanocortin system. Rats were habituated to the test environment and injection procedure and then received intracerebroventicular injection of various combinations of the MCR4 receptor antagonist SR 131716. Food intake and locomotor activity were then recorded for 120 min. When administered alone, SR 141716 and α-MSH dose-dependently attenuated baseline feeding whereas sub-anorectic doses of SR 141716 and α-MSH synergistically attenuated baseline when combined. Δ⁹-Tetrahydrocannabinol-induced feeding was not blocked by α-MSH, whereas SR 141716 dose-dependently attenuated JKC-363-induced feeding. Locomotor activity was not significantly affected by any drug treatment, suggesting that the observed effects on feeding were not due to a nonspecific reduction in motivated behavior. These findings revealed a synergistic interaction between the cannabinoid and melanocortin systems in feeding behavior. These results further suggested that CB₁ receptors are located downstream from melanocortin receptors and CB₁ receptor signaling is necessary to prevent the melanocortin system from altering food intake.
Publication Type: Journal Article
Source of Publication: Endocrinology, 145(7), p. 3224-3231
Publisher: The Endocrine Society
Place of Publication: Chevy Chase, MD, United States
ISSN: 0013-7227
Field of Research (FOR): 111601 Cell Physiology
Socio-Economic Objective (SEO): 970111 Expanding Knowledge in the Medical and Health Sciences
Peer Reviewed: Yes
HERDC Category Description: C1 Refereed Article in a Scholarly Journal
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