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
Article first published online: 3 DEC 2009
© 2009 The Authors. Journal Compilation © 2009 International Society for Neurochemistry
Journal of Neurochemistry
Volume 112, Issue 4, pages 1054–1064, February 2010
How to Cite
Taepavarapruk, P. and Song, C. (2010), 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. Journal of Neurochemistry, 112: 1054–1064. doi: 10.1111/j.1471-4159.2009.06524.x
- Issue published online: 20 JAN 2010
- Article first published online: 3 DEC 2009
- Received June 29, 2009; revised manuscript received November 24, 2009; accepted November 26, 2009.
- memory impairment;
- nerve growth factor
J. Neurochem. (2009) 112, 1054–1064.
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.