Long-chain polyunsaturated fatty acids modulate ...
|Title||Long-chain polyunsaturated fatty acids modulate interleukin-1 beta-induced changes in behavior, monoaminergic neurotransmitters, and brain inflammation in rats|
|Author(s)||Cai Song, Mehar S. Manku, David F. Horrobin|
|Journal||Journal of Nutrition|
|Abstract||Recent evidence has suggested that an imbalance between membrane (n-3) and (n-6) fatty acids may contribute to the etiology of autoimmune and neurodegenerative diseases. In this study, the mechanisms by which eicosapentaenoic acid (EPA), gamma-linolenic acid (GLA), and arachidonic acid (AA) modulate neurotransmitters, behavior, and brain inflammation were evaluated in rats that received central saline or interleukin-1 beta (IL-1) administrations. In rats treated with saline, only the A A-enriched diet significantly increased anxiety-like behavior in the elevated plus maze, which was associated with increased corticosterone secretion. AA also increased the turnover of dopamine (DA), noradrenaline (NA), and serotonin (5-HT) in the amygdala and increased the prostaglandin (PG)E-2 level in the hippocampus, IL-1 administration slowed rat learning in the water maze and increased anxiety-like behavior, changes which were associated with increased homovanillic acid and 5-HT turnover, decreased NA in the hippocampus and amygdala, decreased DA in the frontal cortex, and decreased IL-1 0 in limbic brain regions. Increased corticosterone secretion following IL-1 administration was accompanied by increased NA turnover in the hippocampus (P <0.05) and increased PGE(2) concentration (P < 0.01) in the limbic brain regions. Of the 3 diets tested, only EPA attenuated IL-1-induced behavioral changes (P < 0.05 or 0.01), which was associated with the modulation of EPA on the neuroendocrine and immune changes induced by IL-1. GLA reduced hippocampal PGE(2) concentration in rats given IL-1 (P < 0.01). AA did not counteract any of the changes induced by IL-1. These results suggest that EPA, GLA, and AA play different roles in the neuroendocrine-immune network.|
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