Sophie Laye, Ph.D.
Research Director INRA, Director of NutriNeuro Institute
Unbalanced intake of essential n-3 polyunsaturated fatty acid (PUFAs) is a hallmark of westernized dietary habits, which occur in both developed and developing countries. Epidemiological and clinical data suggest that the consumption of diets poor in n-3 PUA are key in several brain disorders. However, the neurobiological mechanisms underlying dietary n-3 PUFA deficiency and in brain disorders is still poorly known.
The purpose of the work conducted in our team is to understand how dietary lipids influences mood and cognitive disorders. To do so, we use state-of-art lipidomics and transcriptomics analyses, super resolution imaging, electrophysiology and behavior in mice fed with a n-3 PUFA deficient or an isocaloric n-3 PUFA balanced diet. N-3 PUFA deficient diet consumption led to a decrease in docosahexaenoic acid (DHA), the main brain n-3 PUFA, in the hippocampus, the prefrontal cortex and the nucleus accumbens. N-3 deficient mice exhibited an impairment in spatial memory and emotional behaviour (anxiety-like and social behaviour). These modifications were accompanied by a reduction of dendritic length in the hippocampus and prefrontal cortex. Emotional behavioral effects of n-3 PUFA deficiency involve changes in endocannabinoid-dependent synaptic plasticity in the nucleus accumbens. Endocannabinoids are retrograde messengers, which adjust the precise timing of neurotransmitter release from the pre-synapse, thus modulating synaptic efficacy and neuronal activity. In addition, neuroinflammatory pathways were activated in the hippocampus of n-3 PUFA mice. In particular, we found that microglia cell activity is impaired in the hippocampus, with a phagocytic activity towards synapses. Overall, dietary n-3 PUFA deficiency is a risk factor for mood and cognitive disorders through the promotion of neuroinflammation and the alteration of endocannabinoid-dependent synaptic plasticity.
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