Nutritional Omega-3 deficiency abolishes endocannabinoid mediated neuronal functions

Abstract : The corollaries of the obesity epidemic that plagues developed societies are malnutrition and resulting biochemical imbalances. Low levels of essential n-3 polyunsaturated fatty acids (n-3 PUFAs) have been linked to neuropsychiatric diseases, but the underlying synaptic alterations are mostly unknown. We found that lifelong n-3 PUFAs dietary insufficiency specifically ablates long-term synaptic depression mediated by endocannabinoids in the prelimbic prefrontal cortex and accumbens. In n-3 deficient mice, presynaptic cannabinoid CB1 receptors (CB1Rs) normally responding to endocannabinoids were uncoupled from their effector Gi/o-proteins. Finally, the dietary-induced reduction of CB1R functions in mood controlling structures is associated with impaired emotional behavior. These findings identify a plausible synaptic substrate for the behavioral alterations caused by the n-3 PUFAs deficiency often observed in western diets
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Mathieu Lafourcade, Thomas Larrieu, Susana Mato, Anais Duffaud, Marja Sepers, et al.. Nutritional Omega-3 deficiency abolishes endocannabinoid mediated neuronal functions. Nature Neuroscience, Nature Publishing Group, 2011, 〈10.1038/nn.2736〉. 〈hal-00612705〉

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