Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions

Mathieu Lafourcade, Thomas Larrieu, Susana Mato, Anais Duffaud, Marja Sepers, Isabelle Matias, Veronique De Smedt-Peyrusse, Virginie F Labrousse, Lionel Bretillon, Carlos Matute, Rafael Rodríguez-Puertas, Sophie Layé, Olivier J Manzoni
Nat Neurosci. 2011-01-30; 14(3): 345-350
DOI: 10.1038/nn.2736

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1. Nat Neurosci. 2011 Mar;14(3):345-50. doi: 10.1038/nn.2736. Epub 2011 Jan 30.

Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal

Lafourcade M(1), Larrieu T, Mato S, Duffaud A, Sepers M, Matias I, De
Smedt-Peyrusse V, Labrousse VF, Bretillon L, Matute C, Rodríguez-Puertas R, Layé
S, Manzoni OJ.

Author information:
(1)INSERM U862, Physiopathology of Synaptic Plasticity Group, Neurocentre
Magendie, Bordeaux Cedex, France.

Comment in
Nat Neurosci. 2011 Mar;14(3):271-2.

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.

DOI: 10.1038/nn.2736
PMID: 21278728 [Indexed for MEDLINE]

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