Prenatal exposure to vitaminD is thought to be critical for optimal fetal neurodevelopment, yet vitaminDdeficiency is apparent in a growing proportion of pregnant women.
The aim of this study was to determine whether a mouse model of vitaminD-deficiencyaltersfetal neurodevelopment.
FemaleBALB/c mice were placed on either a vitaminD 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.
VitaminDdeficiency during pregnancy reduced fetal crown-rump length and head size. Moreover, lateral ventricle volume was reduced in vitaminD-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 vitaminDdeficiency.
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 vitaminD-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 vitaminD-deficient female foetuses.
Overall, we show that prenatal vitaminD-deficiency leads to alterations in fetalmousebrainmorphology and genes related to neuronal survival, speech and language development, and dopamine synthesis. VitaminD appears to play an important role in mouse neurodevelopment.
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