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首页> 外文期刊>Neuron >Genetically increased cell-intrinsic excitability enhances neuronal integration into adult brain circuits.
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Genetically increased cell-intrinsic excitability enhances neuronal integration into adult brain circuits.

机译：基因增加的细胞内在兴奋性增强了神经元整合到成人脑回路中的能力。

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摘要

New neurons are added to the adult brain throughout life, but only half ultimately integrate into existing circuits. Sensory experience is an important regulator of the selection of new neurons but it remains unknown whether experience provides specific patterns of synaptic input or simply a minimum level of overall membrane depolarization critical for integration. To investigate this issue, we genetically modified intrinsic electrical properties of adult-generated neurons in the mammalian olfactory bulb. First, we observed that suppressing levels of cell-intrinsic neuronal activity via expression of ESKir2.1 potassium channels decreases, whereas enhancing activity via expression of NaChBac sodium channels increases survival of new neurons. Neither of these modulations affects synaptic formation. Furthermore, even when neurons are induced to fire dramatically altered patterns of action potentials, increased levels of cell-intrinsic activity completely blocks cell death triggered by NMDA receptor deletion. These findings demonstrate that overall levels of cell-intrinsic activity govern survival of new neurons and precise firing patterns are not essential for neuronal integration into existing brain circuits.
机译：在整个生命中，新的神经元都会被添加到成人大脑中，但最终只有一半会整合到现有电路中。感觉经验是选择新神经元的重要调节器，但是经验是否提供特定的突触输入模式还是仅对整合至关重要的最低水平的整体膜去极化仍是未知的。为了调查此问题，我们对哺乳动物嗅球中成年神经元的内在电特性进行了遗传修饰。首先，我们观察到通过ESKir2.1钾通道的表达抑制细胞内在神经元活性的水平降低，而通过NaChBac钠通道的表达增强活性则增加了新神经元的存活率。这些调节均不影响突触形成。此外，即使当神经元被激发激发动作电位的模式时，细胞内在活性水平的提高也完全阻断了NMDA受体缺失引发的细胞死亡。这些发现表明，细胞内在活性的总体水平决定着新神经元的存活，精确的放电模式对于将神经元整合到现有的大脑回路中并不是必需的。

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