Vitamin E deficiency induces axonal degeneration in mouse hippocampal neurons

Koji Fukui, Hiroaki Kawakami, Tatsuki Honjo, Reiko Ogasawara, Hirokatsu Takatsu, Tadashi Shinkai, Tatsuro Koike, Shiro Urano

研究成果: Article査読

18 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)377-383
ページ数7
ジャーナルJournal of nutritional science and vitaminology
58
6
DOI
出版ステータスPublished - 2012

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

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