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A.Thomazeau, C.Bosch-Bouju dans Cerebral Cortex

Les apports alimentaires en oméga-3 pendant le développement cérébral sont déterminants pour la facilitation de la LTP hippocampique par les endocannabinoïdes

Le 15 mars 2016

Nutritional n-3 PUFA deficiency abolishes endocannabinoid gating of hippocampal long-term potentiation. Aurore Thomazeau*, Clémentine Bosch-Bouju*, Olivier Manzoni#, Sophie Layé*Authors contributed equally to the study #Authors jointly directed this work. Cerebral Cortex, 2016, 1-9 ; doi : 10.1093/cerco/bhw052


Polyunsaturated fatty acids (PUFAs) are essential fatty acids with crucial role in brain function. PUFAs are of two families, n-3 and n-6 PUFAs, also called omega-3 and omega-6. Maternal n-3 PUFA, especially docosahexaenoic acid (DHA), is critical during perinatal brain development. We previously showed that maternal n-3 PUFA deficiency was strongly impairing endocannabinoid-dependent synaptic plasticity in the prefrontal and in the nucleus accumbens (Lafourcade et al., 2011, Nat Neurosci, 14(3): 345-350). We also demonstrated that perinatal n-3 PUFA deficiency induced strong cognitive impairments (Moranis et al., 2012, BBI, 26:721-731).


 In this study, we investigated whether developmental n-3 PUFA deficiency is impacting on hippocampal synaptic plasticity, since hippocampus is highly implicated in Nutritional n-3 PUFA deficiency abolishes endocannabinoid gating of hippocampal long-term potentiation Aurore Thomazeau*, Clémentine Bosch-Bouju*, Olivier Manzoni#, Sophie Layé# *Authors contributed equally to the study #Authors jointly directed this work Cerebral Cortex, 2016, 1-9 ; doi : 10.1093/cerco/bhw052 synapses in the CA1 region of the hippocampus in weaned pups whose mothers were fed with an n-3 PUFA balanced or n-3 PUFA deficient diet. Normally, endogenous cannabinoids (eCB) produced by the post-synapse dually control network activity by mediating the long-term depression of inhibitory inputs (iLTD) and positively gating NMDAR-dependent long-term potentiation (LTP) of excitatory inputs. We found that both iLTD and LTP were impaired in n-3 PUFA deficient mice. Pharmacological dissection of the underlying mechanism revealed that impairment of NMDAR-dependent LTP was causally linked to and attributable to the ablation of eCB-mediated iLTD and associated to disinhibitory gating of excitatory synapses. The data shed new light on how n-3 PUFAs shape synaptic activity in the hippocampus and provide a new synaptic substrate to the cognitive impairments associated with perinatal n-3 deficiency. This work has been done in collaboration with the team of Dr. Olivier Manzoni (INMED, Marseille) and is founded by ANR MoodFood.

Clémentine Bosch-Bouju /PhD / INRA Laboratoire NutrINeurO /- Nutrition et Neurobiologie Intégrée / clementine.bosch@bordeaux.inra.fr
Dernière mise à jour le 15.03.2016