title: Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs.
abstract: 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.
  
  
  METHODS
  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.
authors.affiliation: Department of Veterinary Disease Biology, University of Copenhagen, Denmark.
authors.forename: Pernille
authors.initials: P
authors.lastname: Tveden-Nyborg
authors.forename: Louise Kruse
authors.initials: LK
authors.lastname: Johansen
authors.forename: Zindy
authors.initials: Z
authors.lastname: Raida
authors.forename: Charlotte Krogh
authors.initials: CK
authors.lastname: Villumsen
authors.forename: Jytte Overgaard
authors.initials: JO
authors.lastname: Larsen
authors.forename: Jens
authors.initials: J
authors.lastname: Lykkesfeldt
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development; D001205:Ascorbic Acid / Q000097:blood; D001206:Ascorbic Acid Deficiency / Q000150:complications* / Q000503:physiopathology; D001522:Behavior, Animal / Q000502:physiology; D015415:Biomarkers / Q000097:blood; D006168:Guinea Pigs; D006624:Hippocampus / Q000166:cytology / Q000254:growth & development*; D018782:Maze Learning / Q000502:physiology; D008568:Memory; D008569:Memory Disorders / Q000209:etiology*; D055495:Neurogenesis; D011897:Random Allocation
chemical_list: D015415:Biomarkers; D001205:Ascorbic Acid