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This Article Full Text Full Text (PDF) All Versions of this Article: 90/3/540    most recent ajcn.2009.27954v1 Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Tveden-Nyborg, P. Articles by Lykkesfeldt, J. PubMed PubMed Citation Articles by Tveden-Nyborg, P. Articles by Lykkesfeldt, J. Agricola Articles by Tveden-Nyborg, P. Articles by Lykkesfeldt, J.

Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs^1,2,3

¹ From the Department of Veterinary Disease Biology (PT-N, LKJ, ZR, CKV, and JL), Faculty of Life Science and the Department of Neuroscience and Pharmacology (JOL), Faculty of Health Science, University of Copenhagen, Copenhagen, Denmark.

² Supported by Danish Research Council grant FSS271-05-0199 (to JL).

³ Address correspondence to J Lykkesfeldt, Department of Veterinary Disease Biology, Faculty of Life Science, University of Copenhagen, 9 Ridebanevej, DK-1870 Frederiksberg C, Denmark. E-mail: jopl{at}life.ku.dk.

Background: The neonatal brain is particularly vulnerable to imbalances in redox homeostasis because of rapid growth and immature antioxidant systems. Vitamin C has been shown to have a key function in the brain, and during states of deficiency it is able to retain higher concentrations of vitamin C than other organs. However, because neurons maintain one of the highest intracellular concentrations of vitamin C in the organism, the brain may still be more sensitive to deficiency despite these preventive measures.

Objective: The objective was to study the potential link between chronic vitamin C deficiency and neuronal damage in newborn guinea pigs.

Design: Thirty 6- to 7-d-old guinea pigs were randomly assigned to 2 groups to receive either a vitamin C–sufficient diet or the same diet containing a low concentration of vitamin C (but adequate to prevent scurvy) for 2 mo. Spatial memory was assessed by the Morris Water Maze, and hippocampal neuron numbers were quantified by stereologic techniques.

Results: The results showed a reduction in spatial memory (P < 0.05) and an increased time to first platform hit (P < 0.05) in deficient animals compared with controls. The deficient animals had a lower total number of neurons in hippocampal subdivisions (dentate gyrus, cornu ammonis 1, and cornu ammonis 2–3) than did the normal controls (P < 0.05).

Conclusions: Our data show that vitamin C deficiency in early postnatal life results in impaired neuronal development and a functional decrease in spatial memory in guinea pigs. We speculate that this unrecognized effect of vitamin C deficiency may have clinical implications for high-risk individuals, such as in children born from vitamin C–deficient mothers.