Ascorbic acid insufficiency impairs spatial memory formation in juvenile AKR1A-knockout mice

DOI Web Site 3 Citations 44 References
  • Kurihara Kazuki
    Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University Department of Anesthesiology, Faculty of Medicine, Yamagata University
  • Homma Takujiro
    Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University
  • Kobayashi Sho
    Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University
  • Shichiri Mototada
    Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST)
  • Fujiwara Hiroki
    Department of Physiology, Faculty of Medicine, Yamagata University
  • Fujii Satoshi
    Department of Physiology, Faculty of Medicine, Yamagata University
  • Yamada Ken-ichi
    Physical Chemistry for Life Science Laboratory, Faculty of Pharmaceutical Sciences, Kyushu University AMED-CREST, Japan Agency for Medical Research and Development
  • Nakane Masaki
    Department of Emergency and Critical Care Medicine, Faculty of Medicine, Yamagata University
  • Kawamae Kaneyuki
    Department of Anesthesiology, Faculty of Medicine, Yamagata University
  • Fujii Junichi
    Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University

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Abstract

<p>AKR1A, an aldo-keto reductase, is involved in the synthesis of ascorbic acid as well as the reduction of a variety of aldehyde compounds. AKR1A−/− mice produce considerably less ascorbic acid (about 10%) compared to AKR1A+/+ mice and require ascorbic acid supplementation in order to breed. To elucidate the roles played by AKR1A in spatial memory, AKR1A−/− male mice were weaned at 4 weeks of age and groups that received ascorbic acid supplementation and no supplementation were subjected to a Morris water maze test. Juvenile AKR1A−/− mice that received no supplementation showed impaired spatial memory formation, even though about 70% of the ascorbic acid remained in the brains of the AKR1A−/− mice at day 7 after weaning. To the contrary, the young adult AKR1A−/− mice at 13–15 weeks of age maintained only 15% of ascorbic acid but showed no significant difference in the spatial memory compared with the AKR1A+/+ mice or ascorbic acid-supplemented AKR1A−/− mice. It is conceivable that juvenile mice require more ascorbic acid for the appropriate level of formation of spatial memory and that maturation of the neural system renders the memory forming process less sensitive to an ascorbic acid insufficiency.</p>

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