Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions.

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Bibliographic Details
Title:	Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions.
Authors:	Lafourcade, Mathieu, Larrieu, Thomas, Mato, Susana, Duffaud, Anais, Sepers, Marja, Matias, Isabelle, De Smedt-Peyrusse, Veronique, Labrousse, Virginie F., Bretillon, Lionel, Matute, Carlos, Rodríguez-Puertas, Rafael, Layé, Sophie, Manzoni, Olivier J.
Source:	Nature Neuroscience. Mar2011, Vol. 14 Issue 3, p345-350. 6p. 5 Graphs.
Subjects:	Omega-3 fatty acids, Obesity, Malnutrition, Neurobehavioral disorders, Prefrontal cortex, Linoleic acid
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 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. [ABSTRACT FROM AUTHOR]
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Database:	Psychology and Behavioral Sciences Collection

Description
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 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. [ABSTRACT FROM AUTHOR]
ISSN:	10976256
DOI:	10.1038/nn.2736