N-3 PUFA improved post-menopausal depression induced by maternal separation and chronic mild stress through serotonergic pathway in rats—effect associated with lipid mediators |
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| Institution: | 1. Department of Food and Nutrition, Hanyang University, Seoul, South Korea;2. UC Davis Genome Center, University of California - Davis, Davis, California 95616, USA;3. Department of Nutrition, University of California - Davis, Davis, California 95616, USA;4. Western Human Nutrition Research Center, Agricultural Research Service, United States Department of Agriculture, Davis, California, USA;1. Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, Yamagata, Japan;2. Department of Immunology, Faculty of Medicine, Yamagata University, Yamagata, Japan;3. Department of Pathological Diagnostics, Faculty of Medicine, Yamagata University, Yamagata, Japan;4. Physical Chemistry for Life Science Laboratory, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan;5. AMED-CREST, Japan Agency for Medical Research and Development, Chiyoda-ku, Tokyo, Japan;6. Miyata Diabetes and Metabolism Clinic, Fukushima-ku, Osaka, Japan;1. Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel;2. Bert Strassburger Lipid Center, Sheba Medical Center, Tel-Hashomer, Israel;3. The Joseph Sagol Neuroscience Center, Sheba Medical Center, Tel-Hashomer, Israel;4. Achva Academic College, Israel;5. School of Psychology, Interdisciplinary Center (IDC) Herzliya, Herzliya, Israel;6. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, NY, USA;7. The Nehemia Rubin Excellence in Biomedical Research – The TELEM Program, Sheba Medical Center, Tel-Hashomer, Israel |
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| Abstract: | Early life maternal separation (MS) increases the vulnerability to depression in rats with chronic mild stress (CMS). N-3 polyunsaturated fatty acids (PUFA) improved depressive behaviors in rats with acute stress; however, their effects on rats with MS+CMS were not apparent. The purpose of the present study was to investigate the hypothesis that lifetime n-3 PUFA supplementation improves post-menopausal depression through the serotonergic and glutamatergic pathways while modulating n-3 PUFA-derived metabolites. Female rats were fed diets of either 0% n-3 PUFA during lifetime or 1% energy n-3 PUFA during pre-weaning, post-weaning, or lifetime periods. Rats were allocated to non-MS or MS groups and underwent CMS after ovariectomy. N-3 PUFA increased brain n-3 PUFA-derived endocannabinoid/oxylipin levels, and reversed depressive behaviors. N-3 PUFA decreased blood levels of adrenocorticotropic hormone and corticosterone, and brain expressions of corticotropin-releasing factor and miRNA-218, which increased the expression of the glucocorticoid receptor. N-3 PUFA decreased the expression of tumor necrosis factor-α, interleukin (IL)-6, IL-1β, and prostaglandin E2, while increased the expression of miRNA-155. N-3 PUFA also increased brainstem serotonin levels and hippocampal expression of the serotonin-1A receptor, cAMP response element-binding protein (CREB), phospho-CREB, and brain-derived neurotrophic factor. However, n-3 PUFA did not affect brain expression of α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor subtype 1, N-methyl-D-aspartate receptor subtype 2B, or miRNA-132. Moreover, n-3 PUFA exposure during lifetime caused greater effects than pre- and post-weaning periods. The present study suggested that n-3 PUFA improved depressive behaviors through serotonergic pathway while modulating the metabolites of n-3 PUFA in post-menopausal depressed rats with chronic stress. |
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