Neuronal Na+/K+-ATPase is responsible for the maintenance of ionic gradient across plasma membrane. In doing so, in a healthy brain, Na+/K+-ATPase activity accounts for nearly half of total brain energy consumption. The α3-subunit containing Na+/K+-ATPase expression is restricted to neurons. Heterozygous mutations within α3-subunit leads to Rapid-onset Dystonia Parkinsonism, Alternating Hemiplegia of Childhood and other neurological and neuropsychiatric disorders. Additionally, proteins such as α-synuclein, amyloid-β, tau and SOD1 whose aggregation is associated to neurodegenerative diseases directly bind and impair α3-Na+/K+-ATPase activity. The review will provide a summary of neuronal α3-Na+/K+-ATPase functional properties, expression pattern, protein-protein interactions at the plasma membrane, biophysical properties (distribution and lateral diffusion). Lastly, the role of α3-Na+/K+-ATPase in neurological and neurodegenerative disorders will be discussed. This article is part of the special issue entitled 'Mobility and trafficking of neuronal membrane proteins'.

中文翻译：

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在健康和疾病中神经元Na + / K + -ATPase的细胞生物学和动力学。

神经元Na + / K + -ATPase负责维持跨质膜的离子梯度。这样，在健康的大脑中，Na + / K + -ATPase活性占大脑总能量消耗的近一半。含有Na + / K + -ATPase表达的α3-亚基仅限于神经元。α3亚基内的杂合突变会导致快速发作的肌张力障碍性帕金森病，儿童交替性偏瘫以及其他神经系统疾病和神经精神疾病。另外，其聚集与神经退行性疾病有关的蛋白质，例如α-突触核蛋白，淀粉样蛋白-β，tau和SOD1，直接结合并损害α3-Na+ / K + -ATPase活性。该综述将概述神经元α3-Na+ / K + -ATPase的功能特性，表达模式，质膜上的蛋白质-蛋白质相互作用，生物物理特性（分布和横向扩散）。最后，将讨论α3-Na+ / K + -ATPase在神经系统疾病和神经退行性疾病中的作用。本文是题为“神经元膜蛋白的移动性和运输”的特刊的一部分。