Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions.
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.
INSERM U862, Physiopathology of Synaptic Plasticity Group, Neurocentre Magendie, Bordeaux Cedex, France., , , , , , , , , , ,
Cannabinoid Receptor Modulators
Fatty Acids, Omega-3
Mice, Inbred C57BL
Receptor, Cannabinoid, CB1
Pub Type(s)Journal Article
Research Support, Non-U.S. Gov't