Effects of maternal dietary zinc deficiency on prenatal and postnatal brain development were investigated in ICR strain mice. From d 1 of pregnancy (E0) until postnatal d 20 (P20), maternal mice were fed experimental diets that contained 1 mg Zn/kg/day (severe zinc deficient, SZD), 5 mg Zn/kg/day (marginal zinc deficient, MZD), 30 mg Zn/kg/day (zinc adequately supplied, ZA) or 100 mg Zn/kg/day (zinc supplemented, ZS and pair-fed, PF). Brains of offspring from these dietary groups were examined at various developmental stages for expression of nestin, an intermediate filament protein found in neural stem cells and young neurons. Immunocytochemistry showed nestin expression in neural tube 10.5 d post citrus (dpc) as well as in the cerebral cortex and neural tube from 10.5 dpc to postnatal d 10 (P10). Nestin immunoreactivities in both brain and neural tube of those zinc-supplemented control groups (ZA, ZS, PF) were stronger than those in zinc-deficient groups (SZD and MZD). Western blot analysis confirmed that nestin levels in pooled brain extracts from each of the zinc-supplemented groups (ZA, ZS, PF) were much higher than those from the zinc-deficient groups (SZD and MZD) from 10.5 dpc to P10. Immunostaining and Western blots showed no detectable nestin in any of the experimental and control group brains after P20. These observations of an association between maternal zinc deficiency and decreased nestin protein levels in brains of offspring suggest that zinc deficiency suppresses development of neural stem cells, an effect which may lead to neuroanatomical and behavioral abnormalities in adults.

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Studies have revealed that the adult mammalian brain has the capacity to regenerate some neurons after cerebral ischemia. And this perspective on neurogenesis adds to the conceptual framework for strategies for the repair of ischemia-induced brain injury, that is, if the effect of ischemia-induced neurogenesis is enhanced, then the recovery of brain function after stroke can be promoted. Neurogenesis is a multistep process that requires the proliferation of neural stem/progenitor cells, migration and that new cells differentiate, survive and integrate into existing neural networks. For that to occur, the same concerted action of various factors is needed, especially transcription factors which regulate the expression of many moleculars and interact with them to promote neurogenesis. This review article gives a brief overview of some transcription factors (NF-κB, Hes, STAT3, AP-1, CREB, HIF1, Pax6, Tcf/Lef, Gli, Sox2, Olig2, Dlx2, TLX, Bmi-1) in ischemia-induced neurogenesis.

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