Reductions of acetylcholine release and nerve growth factor expression are correlated with memory impairment induced by interleukin-1β administrations: effects of omega-3 fatty acid EPA treatment

Authors

  • Pornnarin Taepavarapruk,

    1. Department of Biomedical Sciences, AVC, University of Prince Edward Island, Charlottetown, PE C1A 4P3, Canada
    2. Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, 65000, Thailand
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  • Cai Song

    1. Department of Biomedical Sciences, AVC, University of Prince Edward Island, Charlottetown, PE C1A 4P3, Canada
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Address correspondence and reprint requests to Cai Song, MD, PhD, Department of Biomedical Science, AVC, University of Prince Edward Island and NRC Institute for Nutrisciences and Health, 550 University Ave, Charlottetown, PE, Canada C1A 4P3. E-mail: cai.song@nrc.gc.ca

Abstract

J. Neurochem. (2009) 112, 1054–1064.

Abstract

Interleukin (IL)-1β may play an important role in Alzheimer’s disease. However, the relationships between glucocorticoids and acetylcholine (ACh), and between neurotrophins and ACh in IL-1-induced memory deficits are unknown. While ethyl-eicosapentaenoate (E-EPA) has recently been reported to reduce inflammation and improve memory, cholinergic and neurotrophic mechanisms by which E-EPA improves memory is unclear. This study evaluated: (i) the correlation between ACh release and memory impairment; (ii) the effect of glucocorticoids on ACh release; (iii) the relationship between nerve growth factor (NGF) and inflammation; and (iv) the effects of E-EPA treatment on IL-1β-induced changes. Intracerebroventricular IL-1β administrations produced a significant reduction in hippocampal ACh release in rats fed control diet, which was partially attenuated by mifepristone (RU 486) and completely blocked by IL-1 receptor antagonist. In eight-arm radial maze, significantly less ACh release was correlated with the memory deficits after IL-1β administrations. mRNA expression of hippocampal NGF was lower, whereas IL-1β was higher when compared with controls. E-EPA treatment significantly improved the memory, which was correlated with normalizing ACh release, and expressions of NGF and IL-1β. This study revealed important mechanisms by which IL-1β impairs, while E-EPA improves memory through IL-1-glucocorticoid-ACh release and IL-1-NGF-ACh release pathways.

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