前突触活动调节了轴突初始段的Na(+) 通道分布
Hiroshi Kuba1, Yuki Oichi, Harunori Ohmori
1Career-Path Promotion Unit for Young Life Scientists, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan. kuba@nbiol.med.kyoto-u.ac.jp
Nature
|June 15, 2010
概括
感官剥夺导致轴突初始段 (AIS) 延长,增加神经元刺激能力. 在AIS中这种恒温可塑性可能有助于在听力损失后保持听觉功能.
科学领域:
- 神经科学是一个神经科学.
- 细胞神经科学 细胞神经科学
- 听觉神经科学 听觉神经科学
背景情况:
- 神经回路表现出可塑性,在被剥夺了附带输入时恢复活动.
- 轴突初始段 (AIS) 对于启动神经信号至关重要,但缺乏已知的可塑性.
- 恒常性调节对于在不断变化的条件下维持神经功能至关重要.
研究的目的:
- 为了调查AIS是否经历塑性变化作为对感官剥夺的反应.
- 为了确定AIS可塑性是否有助于神经元刺激性调节.
- 探索AIS可塑性在听力损失后维持神经功能中的作用.
主要方法:
- 听觉输入剥夺在鸟类脑干听觉神经元.
- 测量AIS长度和电压关闭的Na ((+) 通道和AIS定蛋白的分布.
- 评估整个细胞的Na ((+) 电流,膜激发能力和自发发射速率.
主要成果:
- 审计输入的剥夺导致AIS长度在七天内增加了1.7倍.
- 增加的AIS长度与增强的全细胞Na(+) 电流和膜刺激性有关.
- 在听觉输入被剥夺后,自发神经元发射率也增加了.
结论:
- 轴突初始段 (AIS) 呈现同居可塑性,延长以应对感官剥夺.
- AIS的可塑性增加了神经元的刺激性,可能会弥补失去的感官输入.
- 尖端启动部位的可塑性提供了一个神经计算在感觉损失期间精细化的机制.
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