Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs.
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.
Tveden-Nyborg
Pernille
P
Department of Veterinary Disease Biology, University of Copenhagen, Denmark.
Johansen
Louise Kruse
LK
Raida
Zindy
Z
Villumsen
Charlotte Krogh
CK
Larsen
Jytte Overgaard
JO
Lykkesfeldt
Jens
J
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
D015415:Biomarkers; D001205:Ascorbic Acid