Journal
NATURE NEUROSCIENCE
Volume 15, Issue 4, Pages 558-564Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.3053
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Funding
- AVENIR/INSERM
- INSERM-Agence Nationale de la Recherche [ANR-09RDPOC-006-01]
- European Union (REPROBESITY) [HEALTH-F2-2008-223713]
- European Research Council (ENDOFOOD) [ERC-2010-StG-260515]
- Fondation pour la Recherche Medicate
- Region Aquitaine
- Fyssen Foundation
- University of Bordeaux
- Red de Trastornos Adictivos, Instituto de Salud Carlos III [RD07/0001/2001]
- Basque Country Government [GIC07/70-IT-432-07]
- University of the Basque Country UPV/EHU [UFI11/41]
- Comunidad de Madrid [S2010/BMD-2353]
- MICINN [SAF2009-07065, SAF2010-22198-C02-01]
- Ramon y Cajal program
- Deutsche Forschungsgemeinschaft [FOR926]
- CONACyT
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The mammalian brain is one of the organs with the highest energy demands, and mitochondria are key determinants of its functions. Here we show that the type-1 cannabinoid receptor (CB1) is present at the membranes of mouse neuronal mitochondria (mtCB(1)), where it directly controls cellular respiration and energy production. Through activation of mtCB(1) receptors, exogenous cannabinoids and in situ endocannabinoids decreased cyclic AMP concentration, protein kinase A activity, complex I enzymatic activity and respiration in neuronal mitochondria. In addition, intracellular CB1 receptors and mitochondria, mechanisms contributed to endocannabinoid-dependent depolarization-induced suppression of inhibition in the hippocampus. Thus, mtCB(1) receptors directly modulate neuronal energy metabolism, revealing a new mechanism of action of G protein-coupled receptor signaling in the brain.
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