Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

Wang, Fudi; Bian, Wei; Kong, Lin; Zhao, Fa Ji; Guo, Jun; Jing, Nai He

doi:10.1038/sj.cr.7290078

Cited by 50 publications

(29 citation statements)

References 24 publications

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“…The abnormalities were not reversed by dietary zinc supplementation after weaning [3]. Further study showed that the nestin protein levels in the developing brain of zinc-deficient groups were lower than those of zinc-supplemented groups, and the level correlated with the amount of dietary zinc consumed by the mother [4]. These findings suggested that zinc deficiency suppresses development of neural stem cells, an effect which might lead to neuroanatomical and behavioral abnormalities in adults.…”

Section: Introductionmentioning

confidence: 96%

Zinc Distribution and Expression Pattern of ZnT3 in Mouse Brain

Shen

Wang

Zhang

et al. 2007

Biol Trace Elem Res

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To explore the relationship between the zinc distribution and zinc transporter 3 (ZnT3) mRNA expression in the mouse brain, zinc contents and its distribution were determined by synchrotron radiation x-ray fluorescence (SRXRF), and ZnT3 mRNA expression was examined by reverse-transcription polymerase chain reaction and in situ hybridization. The results showed that the zinc contents were not distributed evenly in various brain tissues. The zinc contents in cerebral cortex and hippocampus were nearly 5-10 times higher than that in other neural locations. Correspondingly, ZnT3 mRNA expression was observed in high abundance in the cerebral cortex, hippocampus, and testis, but was not detected in other organs and tissues. In the nervous system, ZnT3 mRNA was detected mainly in hippocampus, cerebral cortex, and spinal ganglion. The present results show the coincident distribution of zinc and ZnT3 mRNA in mouse brain. The high zinc contents might be determined by the high expression of ZnT3. More meaningfully, the results showed the feasibility of applying of SRXRF in examining the distribution of minerals in different organs and tissues. In addition, it was observed for the first time that ZnT3 mRNA was expressed in the facial nucleus. The function of ZnT3 in facial nucleus awaits further study.

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Section: Introductionmentioning

confidence: 96%

Zinc Distribution and Expression Pattern of ZnT3 in Mouse Brain

Shen

Wang

Zhang

et al. 2007

Biol Trace Elem Res

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“…In support of this, ethanol exposure during organogenesis has been demonstrated to inhibit neuronal differentiation and proliferation (29) and cause apoptosis in cell populations, such as the developing neural plate and primitive streak (30). Suppression of normal neural stem cell development has been similarly demonstrated by a deficiency of dietary Zn throughout pregnancy (31,32). This could interfere with subsequent developmental stages (migration or differentiation), leading to major structural changes in the brain.…”

Section: Discussionmentioning

confidence: 99%

Prenatal Zinc Treatment at the Time of Acute Ethanol Exposure Limits Spatial Memory Impairments in Mouse Offspring

2006

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Zinc (Zn) treatment given together with acute ethanol in early pregnancy has previously been demonstrated to protect against physical birth abnormalities in mice. The current study examined whether this Zn treatment (s.c. injection) can also prevent the more subtle cognitive impairments caused by ethanol exposure in early pregnancy. Pregnant C57BL/6J dams were injected with saline (0.85% wt/vol NaCl) or 25% ethanol (0.015 mL/g body weight) intraperitoneally at 0 and 4 h on gestational d (GD) 8. ZnSO 4 (2.5 g Zn/g at 0 h) treatment was administered by s.c. injection immediately following ethanol treatment. Offspring were randomly selected from litters for each of the three treatment groups and were tested at 55 and 70 d of age using a cross-maze water escape task for spatial learning and memory impairments consecutively. No differences were observed between treatments for the spatial learning task. However, young adult mice exposed to ethanol in utero demonstrated impaired spatial memory, with a decrease in correct trials and increased escape latency and incorrect entry measurements, compared with salinetreated controls. In comparison, offspring given s.c. Zn treatment at the time of ethanol exposure were not cognitively impaired, performing at the same level as control mice in the cross-maze escape task. These findings indicate that critically timed Zn administration can limit spatial memory impairments caused by ethanol exposure in early pregnancy. T he teratogenic nature of ethanol has been well documented in humans and experimental animals (1-3). Consumption of ethanol during pregnancy can produce an array of physical abnormalities, including prenatal and/or postnatal growth deficiency and craniofacial dysmorphology (4). However, cognitive and behavioral impairments, such as deficits in attention, learning, and memory (5) are much more commonly observed in children exposed prenatally to ethanol and hence are more significant and costly to both the individual and community. These outcomes result from diverse maternal drinking patterns, ranging from the episodic ЉbingeЉ of large quantities of ethanol over a short time period to chronic ethanol intake.The mechanisms involved in ethanol-related abnormalities are unclear. Although it is likely that many factors are involved, several lines of evidence support fetal Zn deficiency as a major contributing factor to ethanol teratogenicity. First, an adequate supply of Zn to the fetus is critical during pregnancy (6). In rodents, there are similarities in fetal outcome between prenatal Zn deficiency and prenatal ethanol exposure. These include increased fetal resorptions, low birth weight, and birth abnormalities (7-10). These effects are potentiated during organogenesis (GD 7-12 in rodents, weeks 3-9 in humans), a period during early pregnancy critical for development and cell differentiation.Second, studies in rats (11) and in our laboratory using mice demonstrate that acute ethanol exposure in early pregnancy causes fetal Zn deficiency via the induction of ...

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“…Some of the newborn neurons migrate to the granular layer and extend mossy fiber axons, indicating that they are integrated into the functional circuitry of the hippocampus (Gould et al 1999;Markakis andGage 1999, van Praag et al 2002;Joo et al 2007). Recently, it has been reported that maternal zinc deficiency impaired microtubule-associated protein-2 expression and reduced numbers of nestin-positive stem cells in prenatal and postnatal mouse brain (Wang et al 2001;Wang et al 1999). It has also been reported that zinc deficiency impairs neurogenesis by regulating p53-dependent molecular mechanisms (Corniola et al 2008).…”

Section: Introductionmentioning

confidence: 91%

Zinc Deficiency Reduces Neurogenesis Accompanied by Neuronal Apoptosis Through Caspase-Dependent and -Independent Signaling Pathways

et al. 2009

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Dietary zinc deficiency may affect zinc homeostasis in the brain and lead to reductions of neurogenesis and neuronal survival. However, the mechanisms responsible for the effects of zinc deficiency on hippocampal neurogenesis and neuronal death remain obscure. In the present study, young CD-1 mice were fed with zinc-deficient diet (0.85 ppm) for 5 weeks. The vesicular zinc was reduced at CA1 and CA3 regions of the hippocampus in zinc-deficient mice. The significant decreased zinc ions was associated with a reduction in proliferating cells labeled with bromo-deoxyuridine (BrdU) and immature neurons labeled with doublecortin (DCX) immunoreactivity in the dentate gyrus of the hippocampus. The processes of DCX-positive neurons were shortened, and flexuously went through into the granular cell layer in zinc-deficient hippocampus. There was also a conspicuous increase in the number of TUNEL-positive cells in the hippocampus after zinc-deficient diet treatment. Meanwhile, the apoptosis proteins, including Fas, Fas ligand (FasL), apoptosis inducing factor (AIF), and caspase-3, were significantly activated in zinc-deficient mouse hippocampus. These data suggest that chronic treatment with zinc-deficient diet results in reduction in hippocampal neurogenesis and increases neuronal apoptosis, indicating that zinc deficiency is associated with destroying structural plasticity in the hippocampus.

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Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

Cited by 50 publications

References 24 publications

Zinc Distribution and Expression Pattern of ZnT3 in Mouse Brain

Zinc Distribution and Expression Pattern of ZnT3 in Mouse Brain

Prenatal Zinc Treatment at the Time of Acute Ethanol Exposure Limits Spatial Memory Impairments in Mouse Offspring

Zinc Deficiency Reduces Neurogenesis Accompanied by Neuronal Apoptosis Through Caspase-Dependent and -Independent Signaling Pathways

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