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首页> 外文期刊>The European Journal of Neuroscience >Injury-induced neurogenesis in Bax-deficient mice: evidence for regulation by voltage-gated potassium channels.
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Injury-induced neurogenesis in Bax-deficient mice: evidence for regulation by voltage-gated potassium channels.

机译：Bax缺陷小鼠的损伤诱导神经发生：电压门控钾通道调节的证据。

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摘要

Adult neural stem and progenitor cells may help remodel the brain in response to injury. The pro-apoptotic molecule Bax has recently been identified as a key player in adult neural stem cell survival. In Bax-deficient mice that have undergone traumatic brain injury, we find increased numbers of neural progenitor cells in the dentate gyrus and improved remodeling of the hippocampus. Exogenous potassium chloride mimics spreading depression (SD)-like events in vitro, and Bax-deficient neural stem cells proliferate in response to these events more robustly than wild-type neural stem cells. Selective potassium channel blockers interrupt SD-mediated stimulation of stem cells. In addition, the potassium channel Kv4.1 is expressed within neural stem and progenitor cells in the dentate gyrus and is increased in Bax-deficiency. These data suggest that the neuroprotection observed after injury in Bax-deficiency may be due to increased neurogenesis via activation of the Kv4 family of potassium channels.
机译：成年的神经干细胞和祖细胞可能有助于响应损伤而重塑大脑。促凋亡分子Bax最近被确定为成人神经干细胞存活的关键因素。在遭受创伤性脑损伤的Bax缺陷小鼠中，我们发现齿状回中神经祖细胞的数量增加，海马体的重塑得到改善。外源氯化钾在体外模拟散布着抑郁症（SD）的事件，与野生型神经干细胞相比，缺乏Bax的神经干细胞对这些事件的反应更牢固。选择性钾通道阻滞剂中断SD介导的干细胞刺激。此外，钾通道Kv4.1在齿状回的神经干细胞和祖细胞中表达，并在Bax缺乏症中增加。这些数据表明在Bax缺乏的损伤后观察到的神经保护作用可能是由于通过激活Kv4家族的钾离子通道增加了神经发生。

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