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首页> 外文期刊>Hippocampus >Lactational zinc deficiency-induced hippocampal neuronal apoptosis by a BDNF-independent TrkB signaling pathway.
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Lactational zinc deficiency-induced hippocampal neuronal apoptosis by a BDNF-independent TrkB signaling pathway.

机译：乳酸锌缺乏症通过不依赖于BDNF的TrkB信号通路诱导海马神经元凋亡。

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摘要

It is well-known that zinc deficiency leads to neuronal death in the brain. Here we tested the hypothesis that changes in the TrkB signaling pathway are involved in hippocampal neuronal apoptosis of suckling offspring with maternal zinc deficiency. Postpartum mice were fed a zinc-deficient (0.85 ppm) diet and their offspring were used as a lactational zinc deficiency mouse model. At P7, P14, and P21, changes in hippocampal neuronal apoptosis were assessed by Nissl and TUNEL staining. BDNF levels and TrkB neurotrophic signaling were examined using immunoblotting assay. Lactational zinc deficiency resulted in lower levels of p-TrkB and p-ERK, and higher levels of Bax/Bcl-2 and caspase-3 in the hippocampus, suggesting that zinc deficiency-induced low levels of TrkB phosphorylation would abrogate the downstream ERK signaling pathway, leading to hippocampal neuronal apoptosis. Most interestingly, our data showed that the activity of Src, a key molecule for zinc-induced TrkB activation through the BDNF-independent pathway, was inhibited significantly, and the expression levels of BDNF were significantly increased in the hippocampus of suckling mice. The present data indicate that zinc depletion-induced hippocampal neuronal apoptosis is likely through modulation of the TrkB neurotrophic signaling pathway by a BDNF-independent and Src-dependent mechanism, whereas higher expression of BDNF is considered as a protective response, which cannot fully compensate for the injury caused by maternal zinc deficiency.
机译：众所周知，锌缺乏会导致大脑神经元死亡。在这里，我们测试了以下假设：TrkB信号通路的变化与母体锌缺乏的哺乳后代的海马神经元凋亡有关。产后小鼠饲喂缺锌（0.85 ppm）饮食，其后代用作哺乳期缺锌小鼠模型。在P7，P14和P21处，通过Nissl和TUNEL染色评估海马神经元凋亡的变化。使用免疫印迹测定法检查BDNF水平和TrkB神经营养信号。哺乳期锌缺乏导致海马中p-TrkB和p-ERK的水平降低，而Bax / Bcl-2和caspase-3的水平升高，这表明锌缺乏导致的低水平TrkB磷酸化将消除下游ERK信号传导通路，导致海马神经元凋亡。最有趣的是，我们的数据表明，Src是锌诱导的通过BDNF非依赖性途径激活TrkB激活的关键分子，其活性被显着抑制，并且在乳鼠海马中BDNF的表达水平显着增加。目前的数据表明，锌缺乏引起的海马神经元凋亡可能是通过依赖BDNF和Src的机制调节TrkB神经营养信号通路来实现的，而较高的BDNF表达被认为是一种保护性反应，不能完全补偿孕妇缺锌造成的伤害。

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