Extrusion versus diffusion: mechanisms for recovery from sodium loads in mouse CA1 pyramidal neurons
Extrusion versus diffusion: mechanisms for recovery from sodium loads in mouse CA1 pyramidal neurons
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DOI：
10.1113/jp272431
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发表时间：
2016-10
期刊：
影响因子：
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通讯作者：
Miguel A. Mondragão;H. Schmidt;Christian Kleinhans;Julia Langer;K. W. Kafitz;C. Rose
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文献类型：
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作者：
Miguel A. Mondragão;H. Schmidt;Christian Kleinhans;Julia Langer;K. W. Kafitz;C. Rose
神经元的活动导致神经元中局部或整体的钠信号，这取决于突触活动的模式。从全球钠负荷中恢复至关重要的依赖于Na+/K+-ATPase和躯体和树突中完整的能量代谢。对于树突局部钠负荷的恢复，Na+/K+-ATPase本身并不是必需的。相反，恢复主要是由横向扩散介导的，表现出的速度比全球钠信号高10倍。在能量缺乏的短时期内，从局部树枝状钠的增加中恢复仍然是有效的，这表明钠向非刺激区的快速扩散强烈地减少了局部的能量需求。
Neuronal activity causes local or global sodium signalling in neurons, depending on the pattern of synaptic activity. Recovery from global sodium loads critically relies on Na+/K+‐ATPase and an intact energy metabolism in both somata and dendrites. For recovery from local sodium loads in dendrites, Na+/K+‐ATPase activity is not required per se. Instead, recovery is predominately mediated by lateral diffusion, exhibiting rates that are 10‐fold higher than for global sodium signals. Recovery from local dendritic sodium increases is still efficient during short periods of energy deprivation, indicating that fast diffusion of sodium to non‐stimulated regions strongly reduces local energy requirements.