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

Kazuki Kurihara, Takujiro Homma, Sho Kobayashi, Mototada Shichiri, Hiroki Fujiwara, Satoshi Fujii, Kenichi Yamada, Masaki Nakane, Kaneyuki Kawamae, Junichi Fujii

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


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 supple-mentation and no supplementation were subjected to a Morris water maze test. Juvenile AKR1A−/− mice that received no supple-mentation 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.

Original languageEnglish
Pages (from-to)209-216
Number of pages8
JournalJournal of Clinical Biochemistry and Nutrition
Issue number3
Publication statusPublished - Jan 1 2019

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Nutrition and Dietetics
  • Clinical Biochemistry


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