(18-02-11) Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions.

Lafourcade M, Larrieu T, Mato S, Duffaud A, Sepers M, Matias I, De Smedt-Peyrusse V, Labrousse VF, Bretillon L, Matute C, Rodr?guez-Puertas R, Lay? S, Manzoni OJ.
1] INSERM U862, Physiopathology of Synaptic Plasticity Group, Neurocentre Magendie, Bordeaux Cedex, France. [2] INRA UMR 1286, CNRS UMR 5226, Nutrition and Integrative Neurobiology, Bordeaux Cedex, France. [3] These authors contributed equally to this work.
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 CB(1) receptors (CB(1)Rs) normally responding to endocannabinoids were uncoupled from their effector G(i/o) proteins. Finally, the dietary-induced reduction of CB(1)R functions in mood-controlling structures was associated with impaired emotional behavior. These findings identify a plausible synaptic substrate for the behavioral alterations caused by the n-3 PUFAs deficiency that is often observed in western diets.

Source: Nat Neurosci. 2011 Jan 30.

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