(20-12-12) Omega-3 fatty acids deficiency aggravates glutamatergic synapse and astroglial ageing in the rat hippocampal CA1.

Latour A, Grintal B, Champeil-Potokar G, Hennebelle M, Lavialle M, Potier B, Billard JM, Vancassel S, Denis I.
Source
NuReLiCe, INRA, 78352, Jouy-en-Josas, France.
Abstract
Epidemiological data suggest that a poor ?3 status favored by the low ?3/?6 polyunsaturated fatty acids ratio in western diets contributes to cognitive decline in the elderly, but mechanistic evidence is lacking. We therefore explored the impact of ?3 deficiency on the evolution of glutamatergic transmission in the CA1 of the hippocampus during ageing by comparing 4 groups of rats aged 6 to 22 months fed ?3-deficient or ?3/?6-balanced diets from conception to sacrifice: Young ?3 Balanced (YB) or Deficient (YD), Old ?3 Balanced (OB) or Deficient (OD) rats. ?3 deficiency induced a 65% decrease in the amount of docosahexaenoic acid (DHA, the main ?3 in cell membranes) in brain phospholipids, but had no impact on glutamatergic transmission and astroglial function in young rats. Ageing induced a 10% decrease in brain DHA, a 35% reduction of synaptic efficacy (fEPSP/PFV) due to decreased pre-synaptic glutamate release, and a 30% decrease in the astroglial glutamate uptake associated to a marked astrogliosis (+100% GFAP). The ?3 deficiency further decreased these hallmarks of ageing (OD vs OB rats: -35% fEPSP/PFV p<0.05, -15% astroglial glutamate uptake p<0.001, +30% GFAP p<0.01). This cannot be attributed to aggravation of the brain DHA deficit because the brains of OD rats had more DHA as those of YD rats. Thus ?3 deficiency worsens the age-induced degradation of glutamatergic transmission and its associated astroglial regulation in the hippocampus. ? 2012 The Authors Aging Cell ? 2012 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.

Source: Aging Cell. 2012 Oct 31. doi: 10.1111/acel.12026

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