Redistribution of Kv1 and Kv7 enhances neuronal excitability during structural axon initial segment plasticity
Redistribution of Kv1 and Kv7 enhances neuronal excitability during structural axon initial segment plasticity
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DOI：
10.1038/ncomms9815
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发表时间：
2015-11-01
影响因子：
16.6
通讯作者：
Adachi, Ryota
中科院分区：
文献类型：
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作者：
Kuba, Hiroshi;Yamada, Rei;Adachi, Ryota
轴突初始段是神经元的触发区，其结构可塑性是调控神经元活动的有力手段。在这里，我们表明AIS的可塑性并不局限于结构变化；它也发生在离子通道表达的变化中，这大大增强了调节的功效。在禽类耳蜗核中，通过去除耳蜗来剥夺传入输入延长了AIS，同时将AIS的主要Kv通道从Kv1.1切换到Kv7.2。由于Kv7.2激活动力学缓慢，Kv通道的重新分配降低了动作电位启动时延长AIS处的分流电导，有效增强了被剥夺神经元的兴奋性。结果表明，AIS的功能可塑性与结构可塑性协同工作，补偿传入输入的损失，维持耳蜗切除听力损失后听觉回路的稳态。
Structural plasticity of the axon initial segment (AIS), the trigger zone of neurons, is a powerful means for regulating neuronal activity. Here, we show that AIS plasticity is not limited to structural changes; it also occurs as changes in ion-channel expression, which substantially augments the efficacy of regulation. In the avian cochlear nucleus, depriving afferent inputs by removing cochlea elongated the AIS, and simultaneously switched the dominant Kv channels at the AIS from Kv1.1 to Kv7.2. Due to the slow activation kinetics of Kv7.2, the redistribution of the Kv channels reduced the shunting conductance at the elongated AIS during the initiation of action potentials and effectively enhanced the excitability of the deprived neurons. The results indicate that the functional plasticity of the AIS works cooperatively with the structural plasticity and compensates for the loss of afferent inputs to maintain the homeostasis of auditory circuits after hearing loss by cochlea removal.