n-3 PUFA status affects expression of genes involved in neuroenergetics differently in the fronto-parietal cortex compared to the CA1 area of the hippocampus: Effect of rest and neuronal activation in the rat

• Published in: Prostaglandins, leukotrienes and essential fatty acids leukotrienes and essential fatty acids, 2012-06, Vol.86 (6), p.211-220
• Main Authors: Harbeby, Emilie, Jouin, Mélanie, Alessandri, Jean-Marc, Lallemand, Marie-Sylvie, Linard, Alain, Lavialle, Monique, Huertas, Alain, Cunnane, Stephen C, Guesnet, Philippe
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - metabolism; Advanced Basic Science; Animals; ATP synthase; Cerebral cortex; Cerebral Cortex - metabolism; Endocrinology & Metabolism; Enriched environment; Fatty Acids, Omega-3 - metabolism; Female; Glucose metabolism; Glucose Transporter Type 1 - genetics; Glucose Transporter Type 1 - metabolism; Hippocampus; Hippocampus - metabolism; Life Sciences; n-3 Fatty acids; Neurons - metabolism; Parietal Lobe - metabolism; Rats; Rats, Wistar; Taqman Low Density Array (TLDA); Transporter GLUT1
• ISSN: 0952-3278; 1532-2823
• DOI: 10.1016/j.plefa.2012.04.008

Abstract n-3 Polyunsaturated fatty acids (PUFA) support whole brain energy metabolism but their impact on neuroenergetics in specific brain areas and during neuronal activation is still poorly understood. We tested the effect of feeding rats as control, n-3 PUFA-deficient diet, or docosahexaenoic acid (DHA)-supplemented diet on the expression of key genes in fronto-parietal cortex and hippocampal neuroenergetics before and after neuronal stimulation (activated) by an enriched environment. Compared to control rats, n-3 deficiency specifically repressed GLUT1 gene expression in the fronto-parietal cortex in basal state and also during neuronal activation which specifically stimulated GLUT1. In contrast, in the CA1 area, n-3 deficiency improved the glutamatergic synapse function in both neuronal states (glutamate transporters, Na+ /K+ ATPase). DHA supplementation induced overexpression of genes encoding enzymes of the oxidative phosphorylation system and the F1F0 ATP synthase in the CA1 area. We conclude that n-3 deficiency repressed GLUT1 gene expression in the cerebral cortex, while DHA supplementation improved the mitochondrial ATP generation in the CA1 area of the hippocampus.