Abstract

We have previously shown that the drop in N-methyl-D-aspartate (NMDA)-induced seizure threshold caused by nutritional magnesium deprivation responded well to the w-3 polyunsaturated fatty acid (PUFA) alpha-linolenate (ALA) (5% rapeseed oil) diet when compared to w-6 PUFA diet. In the present work, kainate-induced seizures are shown to be also exacerbated by magnesium deprivation. ALA diet better attenuates this seizure exacerbation when compared to the non-ALA diet. The reversion of the drop in kainate seizure threshold induced in these conditions by magnesium administration was, however, better under the non-ALA diet in comparison with the ALA diet. Taken as a whole, present data indicate that kainate like NMDA brain injury is attenuated by ALA diet. On the other hand, the relative failure of ALA diet to potentiate reversion induced by magnesium might suggest that magnesium and ALA protections are not additive.

Highlights

  • 2010; Pages et al, 2011)

  • Chronic magnesium deprivation based on a vegetable oil diet devoided of v-3 polyunsaturated fatty acids (v3PUFA) in mice was recently shown to represent an interesting nutritional model for in vivo exacerbated NMDA receptor function which responds remarkably to acute magnesium supply, adding experimental evidence that magnesium administration is a promising approach of glutamate-mediated brain disorders (Maurois et al, 2009)

  • The drop induced by magnesium deficiency in the threshold to kainateinduced seizures was partly reversed by acute intraperitoneal administrations of 28 mg/kg magnesium which increased by 213 and 154% the kainate seizure threshold of mice given a magnesiumdeficient diet supplemented with corn: sunflower (ALA poor) and rapeseed (ALA rich) oils, respectively

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Summary

Introduction

2010; Pages et al, 2011). Chronic magnesium deprivation based on a vegetable oil diet devoided of v-3 polyunsaturated fatty acids (v3PUFA) (diet containing 5% corn/sunflower oil) in mice was recently shown to represent an interesting nutritional model for in vivo exacerbated NMDA receptor function (reduction of NMDA seizures threshold) which responds remarkably to acute magnesium supply, adding experimental evidence that magnesium administration is a promising approach of glutamate-mediated brain disorders (Maurois et al, 2009). Many recent studies have documented the beneficial effects of v-3 PUFA on cardiovascular diseases (Heurteaux et al, 2006) and neurological disorders (Vreugdenhil et al, 1996; Xiao and Li, 1999; Lauritzen et al, 2000; Kim et al, 2001; Blondeau et al, 2009; Delattre et al, 2010) including epilepsy (Heurteaux et al, 2006; Pages et al, 2011) These studies mainly focused on beneficial effects of docosahexaenoic acid (DHA) and eicosapentaenoic (EPA) acids, and to a less extent on the effects of alpha-linolenic acid (ALA) (18:3 n-3). The aim of the present study was to study whether dietary rapeseed oil could protect mice against kainate-induced seizures in adult mice fed magnesium deficient (35 ppm) or normal magnesium containing (900 ppm) diets containing 5% lipids brought by either corn: sunflower oil or rapeseed oil

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