The Na⁺/K⁺-ATPase is a transmembrane ion pump that has a critical homeostatic role within every mammalian cell; however, it is vulnerable to the effects of increased oxidative stress. Understanding how expression of this transporter is influenced by oxidative stress may yield insight into its role in the pathophysiology of neurological and neuropsychiatric diseases. In this study we investigated whether increased oxidative stress could influence Na⁺/K⁺-ATPase expression in various brain regions of mice. We utilized two different models of oxidative stress: a behavioural chronic unpredictable stress protocol and the Aldh2^−/− mouse model of oxidative stress-based and age-related cognitive impairment. We identified distinct regional baseline mRNA and protein expression patterns of the Na⁺/K⁺-ATPase α1 and α3 isoforms within the neocortex, hippocampus, and brainstem of wildtype mice. Consistent with previous studies, there was a higher proportion of α3 expression relative to α1 in the brainstem versus neocortex, but a higher proportion of α1 expression relative to α3 in the neocortex versus the brainstem. The hippocampus had similar expression levels of both α1 and α3. Despite increased staining for oxidative stress in higher brain, no differences in α1 or α3 expression were noted in Aldh2^−/− mice versus wildtype, or in mice exposed to a 28-day chronic unpredictable stress protocol. In both models of oxidative stress, gene and protein expression of Na⁺/K⁺-ATPase α1 and α3 isoforms within the higher and lower brain was remarkably stable. Thus, Na⁺/K⁺-ATPase function previously reported as altered by oxidative stress is not through induced changes in the expression of pump isoforms.

Na ⁺ / K ⁺ -ATPase是一种跨膜离子泵，在每个哺乳动物细胞中都具有至关重要的稳态作用。但是，它容易受到氧化应激增加的影响。了解这种转运蛋白的表达如何受到氧化应激的影响，可能会深入了解其在神经系统疾病和神经精神疾病的病理生理中的作用。在这项研究中，我们调查了氧化应激的增加是否会影响小鼠各个大脑区域的Na ⁺ / K ⁺ -ATPase表达。我们利用了两种不同的氧化应激模型：行为慢性不可预测的应激方案和Aldh2 ^-/-基于氧化应激和年龄相关的认知障碍的小鼠模型。我们确定了野生型小鼠新皮层，海马和脑干内Na ⁺ / K ⁺ -ATPaseα1和α3亚型的不同区域基线mRNA和蛋白质表达模式。与先前的研究一致，相对于新皮层，在脑干中相对于α1的α3表达比例较高，但是相对于新皮层在脑干中相对于α3的α1表达比例较高。海马α1和α3的表达水平相似。尽管高等脑部的氧化应激染色增加，但Aldh2 ^-/-中未观察到α1或α3表达的差异小鼠与野生型的比较，或暴露于28天慢性不可预测的应激方案的小鼠中。在这两种氧化应激模型中，上下大脑中Na ⁺ / K ⁺ -ATPaseα1和α3亚型的基因和蛋白质表达非常稳定。因此，先前报道的被氧化应激改变的Na ⁺ / K ⁺ -ATPase功能不是通过泵异型表达的诱导变化。