Food and Behaviour Research

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Maternal vitamin D deficiency alters fetal brain development in the BALB/c mouse.

Hawes JE, Tesic D, Whitehouse AJ, Zosky GR, Smith JT, Wyrwoll CS (2015) Behav Brain Res. 286 192-200 Elsevier B.V.

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Abstract:

Prenatal exposure to vitamin D is thought to be critical for optimal fetal neurodevelopment, yet vitamin D deficiency is apparent in a growing proportion of pregnant women.

The aim of this study was to determine whether a 
mouse model of vitamin D-deficiency alters fetal neurodevelopment.

Female
BALB/c mice were placed on either a vitamin D control (2195IU/kg) or deficient (0IU/kg) diet for 5 weeks prior to and during pregnancy. Fetal brains were collected at embryonic day (E) 14.5 or E17.5 for morphological and gene expression analysis. 

Vitamin D deficiency during pregnancy reduced fetal crown-rump length and head size. Moreover, lateral ventricle volume was reduced in vitamin D-deficient foetuses.
Expression of neurotrophin genes 
brain-derived neurotrophic factor (Bdnf) and transforming growth factor-β1 (Tgf-β1) was altered, with Bdnf reduced at E14.5 and increased at E17.5 following vitamin D deficiency

Brain expression of forkhead box protein P2 (Foxp2), a gene known to be important in human speech and language, was also altered. Importantly, Foxp2 immunoreactive cells in the developing cortex were reduced in vitamin D-deficient female foetuses.

At E17.5, 
brain tyrosine hydroxylase (TH) gene expression was reduced in females, as was TH protein localization (to identify dopamine neurons) in the substantia nigra of vitamin D-deficient female foetuses.

Overall, we show that prenatal 
vitamin D-deficiency leads to alterations in fetal mouse brainmorphology and genes related to neuronal survival, speech and language development, and dopamine synthesis. Vitamin D appears to play an important role in mouse neurodevelopment.