Brain protection by rapeseed oil in magnesium-deficient mice

Abstract

Diets given for 30 days with various mono-(MUFA) and poly-(PUFA) unsaturated fatty acid contents were evaluated for brain protection in magnesium-deficient mice: a commercial and three synthetic diets (n-6PUFA, n-3PUFA and MUFA-based chows enriched with 5% corn/sunflower oils 1:3, with 5% rapeseed oil and with 5% high oleic acid sunflower oil/sunflower oil 7:3, respectively). Unlike magnesium deprivation, they induced significant differences in brain and erythrocyte membrane phospholipid fatty acid compositions. n-3PUFA but not other diets protected magnesium-deficient mice against hyperactivity and moderately towards maximal electroshock- and NMDA-induced seizures. This diet also inhibited audiogenic seizures by 50%, preventing animal deaths. Because, like n-6PUFA diet, matched control MUFA diet failed to induce brain protections, alpha-linolenate (ALA) rather than reduced n-6 PUFA diet content is concluded to cause n-3PUFA neuroprotection. Present in vivo data also corroborate literature in vitro inhibition of T type calcium channels by n-3 PUFA, adding basis to ALA supplementation in human anti-epileptic/neuroprotective strategies.

Rapeseed oil and magnesium manipulations affect the seizure threshold to kainate in mice

“…ALA is supplied with diet via different vegetal origins: it represents 9% of the rapeseed oil composition, which also contains 60% monounsaturated fatty acids (MUFA) (18:1 fatty acid) and 20% v6PUFA. Its v6/v3 ratio is low (close to 3) contrasting with the high ratio (more than 80) characterizing corn:sunflower oils which contain 28% MUFA, 56% v-6 PUFA and 0.6% v-3 PUFA (Pages et al, 2011). Diet containing 5% rapeseed oil (rich in v-3 alpha-linolenate (ALA) improves protection against experimental seizures including NMDA induced seizures to a higher extent than diet containing 5% corn/sunflower oil devoided of v-3 PUFA (Pages et al, 2011), supporting modulation of glutamate neurotransmission by v-3 PUFAs.…”

“…Its v6/v3 ratio is low (close to 3) contrasting with the high ratio (more than 80) characterizing corn:sunflower oils which contain 28% MUFA, 56% v-6 PUFA and 0.6% v-3 PUFA (Pages et al, 2011). Diet containing 5% rapeseed oil (rich in v-3 alpha-linolenate (ALA) improves protection against experimental seizures including NMDA induced seizures to a higher extent than diet containing 5% corn/sunflower oil devoided of v-3 PUFA (Pages et al, 2011), supporting modulation of glutamate neurotransmission by v-3 PUFAs. Glutamate-driven excitatory synaptic neurotransmission in the mammalian central nervous system is also mediated in major part by receptors other than the NMDA-type receptor and 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 mice, this particular nutritional animal model may be exploited for its susceptibility to audiogenic seizures to evaluate in vivo brain activity of anticonvulsant, neuroprotective, and antiinflammatory/antioxidant compounds (Bac et al, 1998;Vamecq et al, 2003;Maurois et al, 2008;Maurois et al, 2009;Pages et al, 2010;Vamecq et al, 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 also 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 effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

“…The percentage of GluR2 subunit can be increased during brain ischemia-reperfusion, thus significantly depress calcium permeability of AMPAR, leading to high ion influx and severe neuron damage [11][12][13]. NMDA receptor contains NR1, NR2, NR3 and NR4 subunits, among which NR2B contributes to a vital function in ischemiainduced neuronal damage [14,15]. Dexmedetomidine (Dex) is a type of selective α2-adernoglandin receptor agonist, and has been used as anesthetics or sedatives for critical patients.…”