Nutritional n-3 PUFA Deficiency Abolishes Endocannabinoid Gating of Hippocampal Long-Term Potentiation
Cereb. Cortex. 2016-03-05; : bhw052
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1. Cereb Cortex. 2017 Apr 1;27(4):2571-2579. doi: 10.1093/cercor/bhw052.
Nutritional n-3 PUFA Deficiency Abolishes Endocannabinoid Gating of Hippocampal
Thomazeau A(1)(2), Bosch-Bouju C(1)(2), Manzoni O(3)(4)(5), Layé S(1)(2).
(1)Nutrition et Neurobiologie Intégrée, UMR 1286, INRA, F-33000 Bordeaux, France.
(2)Nutrition et Neurobiologie Intégrée, UMR 1286, Bordeaux University, F-33000
(5)INMED UMR S 901, Marseille 13009, France.
Maternal n-3 polyunsaturated fatty acids (PUFAs), especially docosahexaenoic
acid, is critical during perinatal brain development. How early postnatal n-3
PUFA deficiency impacts on hippocampal synaptic plasticity is mostly unknown.
Here we compared activity-dependent plasticity at excitatory and inhibitory
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.
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PMID: 26946127 [Indexed for MEDLINE]