Zinc Deficiency Reduces Neurogenesis Accompanied by Neuronal Apoptosis Through Caspase-Dependent and -Independent Signaling Pathways
Zinc Deficiency Reduces Neurogenesis Accompanied by Neuronal Apoptosis Through Caspase-Dependent and -Independent Signaling Pathways
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缺锌通过依赖 Caspase 和独立的信号通路减少神经发生，并伴有神经元凋亡
DOI：
10.1007/s12640-009-9072-7
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发表时间：
2009-11-01
影响因子：
3.7
通讯作者：
Wang, Zhan-You
中科院分区：
文献类型：
--
作者：
Gao, Hui-Ling;Zheng, Wei;Wang, Zhan-You
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.
