Feeding induced by cannabinoids is mediated independently of the melanocortin system.
| Autor: | Sinnayah P; Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Portland, Oregon, United States of America., Jobst EE, Rathner JA, Caldera-Siu AD, Tonelli-Lemos L, Eusterbrock AJ, Enriori PJ, Pothos EN, Grove KL, Cowley MA |
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| Jazyk: | angličtina |
| Zdroj: | PloS one [PLoS One] 2008 May 21; Vol. 3 (5), pp. e2202. Date of Electronic Publication: 2008 May 21. |
| DOI: | 10.1371/journal.pone.0002202 |
| Abstrakt: | Background: Cannabinoids, the active components of marijuana, stimulate appetite, and cannabinoid receptor-1 (CB1-R) antagonists suppress appetite and promote weight loss. Little is known about how CB1-R antagonists affect the central neurocircuitry, specifically the melanocortin system that regulates energy balance. Methodology/principal Findings: Here, we show that peripherally administered CB1-R antagonist (AM251) or agonist equally suppressed or stimulated feeding respectively in A(y) , which lack a functional melanocortin system, and wildtype mice, demonstrating that cannabinoid effects on feeding do not require melanocortin circuitry. CB1-R antagonist or agonist administered into the ventral tegmental area (VTA) equally suppressed or stimulated feeding respectively, in both genotypes. In addition, peripheral and central cannabinoid administration similarly induced c-Fos activation in brain sites suggesting mediation via motivational dopaminergic circuitry. Amperometry-detected increases in evoked dopamine (DA) release by the CB1-R antagonist in nucleus accumbens slices indicates that AM251 modulates DA release from VTA terminals. Conclusions/significance: Our results demonstrate that the effects of cannabinoids on energy balance are independent of hypothalamic melanocortin circuitry and is primarily driven by the reward system. |
| Databáze: | MEDLINE |
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