Vitamin E deficiency induces axonal degeneration in mouse hippocampal neurons
2012
Fukui, K. ((Shibaura Institute of Technology, Saitama (Japan). College of Systems Engineering and Sciences, Department of Bioscience and Engineering, Physiological Chemistry Laboratory), (Shibaura Institute of Technology, Saitama (Japan). Research Organization for Advanced Engineering, Life Support Technology Research Center)) | Kawakami, H. | Honjo, T. | Ogasawara, R. | Takatsu, H. | Shinkai, T. | Koike, T. | Urano, S.
Several lines of evidence demonstrate the relationship between vitamin E deficiency and cognitive dysfunction in rodent models, but little is known about the underlying mechanisms. In this study, we found axonal injury in the hippocampal CA1 region of vitamin E-deficient and normal old mice using immunohistochemical assay. The number of cells in the hippocampal CA1 region of vitamin E-deficient mice and normal old mice was significantly lower than in normal young mice. It is well known that collapsin response mediator protein (CRMP)-2 plays a crucial role in the maintenance of axonal conditions. The expressions of CRMP-2 in the cerebral cortex and hippocampus of vitamin E-deficient mice were significantly lower than both the regions of normal ones. In normal old mice, the expression of CRMP-2 in the cerebral cortex was significantly lower than in the normal ones. In addition, the appearance of microtubule-associated protein (MAP)-light chain 3 (LC3), a major index of autophagy, was higher in the cerebral cortex and hippocampus of vitamin E-deficient mice than in normal young and old mice. These results indicate that axonal degeneration is induced in living tissues, but not cultured cells, and that changes in CRMP-2 and MAP-LC3 may underlie vitamin E-deficiency-related axonal degeneration.
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