Nature：内在的神经弹性来源-AIS（附全文）

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9 F1 Y, w' Z7 k1 \' i位于每个神经纤维根部的“轴突起始段” (AIS)（在那里，成簇的钠通道产生动作势，后者随后沿轴突传播），是从事神经可激发性之性质研究的神经科学家的关注焦点。作为一个神经脉冲的来源，它似乎是调控神经活动的一个逻辑点。本期Nature上两篇论文证实，AIS是一个内在的神经弹性来源。: V$ \) L) x2 Z
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Matthew Grubb 和 Juan Burrone发现，电活动可逆地改变AIS在培养的海马神经元中的位置。他们提出，由此所导致的内在可激发性的增加在发育过程中可能会微调神经可激发性，同时也为癫痫的控制指出了潜在目标。Hiroshi Kuba、Yuki Oichi 和Harunori Ohmori发现，在消除了声音刺激的鸟听觉神经元中，AIS的尺寸增加。同样，内在可激发性会增加、并且可能有助于听觉通道的维持。这样的神经弹性也许可补偿某些形式的失聪。
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Nature doi:10.1038/nature09160
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  m" t8 v2 i: \: SActivity-dependent relocation of the axon initial segment fine-tunes neuronal excitability
& ?& K: Q- ~( V: A  ~; \Matthew S. Grubb& Juan Burrone
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In neurons, the axon initial segment (AIS) is a specialized region near the start of the axon that is the site of action potential initiation1, 2, 3, 4, 5, 6. The precise location of the AIS varies across and within different neuronal types7, 8, and has been linked to cells’ information-processing capabilities8; however, the factors determining AIS position in individual neurons remain unknown. Here we show that changes in electrical activity can alter the location of the AIS. In dissociated hippocampal cultures, chronic depolarization with high extracellular potassium moves multiple components of the AIS, including voltage-gated sodium channels, up to 17?μm away from the soma of excitatory neurons. This movement reverses when neurons are returned to non-depolarized conditions, and depends on the activation of T- and/or L-type voltage-gated calcium channels. The AIS also moved distally when we combined long-term LED (light-emitting diode) photostimulation with sparse neuronal expression of the light-activated cation channel channelrhodopsin-2; here, burst patterning of activity was successful where regular stimulation at the same frequency failed. Furthermore, changes in AIS position correlate with alterations in current thresholds for action potential spiking. Our results show that neurons can regulate the position of an entire subcellular structure according to their ongoing levels and patterns of electrical activity. This novel form of activity-dependent plasticity may fine-tune neuronal excitability during development.