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首页> 外文期刊>Developmental cell >BAK Alters Neuronal Excitability and Can Switch from Anti-to Pro-Death Function during Postnatal Development
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BAK Alters Neuronal Excitability and Can Switch from Anti-to Pro-Death Function during Postnatal Development

机译：BAK会改变神经元兴奋性，并且在产后发育过程中可从抗死亡功能转为死亡前功能

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摘要

BAK is a pro-apoptotic BCL-2 family protein that localizes to mitochondria. Here we evaluate the function of BAK in several mouse models of neuronal injury including neuronotropic Sindbis virus infection, Parkinson's disease, ischemia/stroke, and seizure. BAK promotes or inhibits neuronal death depending on the specific death stimulus, neuron subtype, and stage of postnatal development. BAK protects neurons from excitotoxicity and virus infection in the hippocampus. As mice mature, BAK is converted from anti-to prodeath function in virus-infected spinal cord neurons. In addition to regulating cell death, BAK also protects mice from kainate-induced seizures, suggesting a possible role in regulating synaptic activity. BAK can alter neurotamsmitter release in a direction consistent with its protective effects on neurons and mice. These findings suggest that BAK inhibits cell death by modifying neuronal excitability.
机译：BAK是一种促凋亡的BCL-2家族蛋白，位于线粒体中。在这里，我们评估了BAK在多种神经元损伤小鼠模型中的功能，其中包括神经营养性辛德比斯病毒感染，帕金森氏病，局部缺血/中风和癫痫发作。 BAK根据特定的死亡刺激，神经元亚型和产后发育阶段来促进或抑制神经元死亡。 BAK保护神经元免受海马的兴奋性毒性和病毒感染。随着小鼠的成熟，BAK在病毒感染的脊髓神经元中从抗死亡功能转变为前代功能。除了调节细胞死亡，BAK还可以保护小鼠免受海藻酸盐诱导的癫痫发作的影响，提示其可能在调节突触活动中发挥作用。 BAK可以在与其对神经元和小鼠的保护作用一致的方向上改变神经填塞剂的释放。这些发现表明，BAK通过修饰神经元兴奋性来抑制细胞死亡。

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