Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs

• Published in: The American journal of clinical nutrition 2009-09, Vol.90 (3), p.540-546
• Main Authors: Tveden-Nyborg, Pernille, Johansen, Louise Kruse, Raida, Zindy, Villumsen, Charlotte Krogh, Larsen, Jytte Overgaard, Lykkesfeldt, Jens
• Format: Article
• Language: English
• Subjects: animal models; Animals; Animals, Newborn - growth & development; ascorbic acid; Ascorbic Acid - blood; Ascorbic Acid Deficiency - complications; Ascorbic Acid Deficiency - physiopathology; Babies; Behavior, Animal - physiology; Biological and medical sciences; Biomarkers - blood; Brain; experimental diets; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Guinea Pigs; hippocampus; Hippocampus - cytology; Hippocampus - growth & development; maternal nutrition; Maze Learning - physiology; Memory; Memory Disorders - etiology; neonates; Neurogenesis; Neurons; postnatal development; Random Allocation; Rodents; spatial memory; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Vitamin C; vitamin deficiencies; Vitamin deficiency
• ISSN: 0002-9165; 1938-3207
• DOI: 10.3945/ajcn.2009.27954

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.