Previously it was shown that for reduction of anxiety and stress of experimental animals, preventive handling seems to be one of the most effective methods. The present study was oriented on Na,K-ATPase, a key enzyme for maintaining proper concentrations of intracellular sodium and potassium ions. Malfunction of this enzyme has an essential role in the development of neurodegenerative diseases. It is known that this enzyme requires approximately 50% of the energy available to the brain. Therefore in the present study utilization of the energy source ATP by Na,K-ATPase in the frontal cerebral cortex, using the method of enzyme kinetics was investigated. As a model of neurodegeneration treatment with trimethyltin (TMT) was applied. Daily handling (10 min/day) of healthy rats and rats suffering neurodegeneration induced by administration of TMT in a dose of (7.5 mg/kg), at postnatal days 60–102 altered the expression of catalytic subunits of Na,K-ATPase as well as kinetic properties of this enzyme in the frontal cerebral cortex of adult male Wistar rats. In addition to the previously published beneficial effect on spatial memory, daily treatment of rats was accompanied by improved maintenance of sodium homeostasis in the frontal cortex. The key system responsible for this process, Na,K-ATPase, was able to utilize better the energy substrate ATP. In rats, manipulation of TMT-induced neurodegeneration promoted the expression of the α2 isoform of the enzyme, which is typical for glial cells. In healthy rats, manipulation was followed by increased expression of the α3 subunit, which is typical of neurons.

先前的研究表明，为了减少实验动物的焦虑和压力，预防性处理似乎是最有效的方法之一。本研究的重点是 Na,K-ATPase，它是维持细胞内钠离子和钾离子适当浓度的关键酶。这种酶的故障在神经退行性疾病的发展中具有重要作用。众所周知，这种酶需要大脑可用能量的大约 50%。因此，在本研究中，利用酶动力学的方法研究了前额大脑皮层中Na，K-ATP酶对能量源ATP的利用。应用三甲基锡 (TMT) 作为神经变性治疗的模型。在出生后第 60-102 天，每天处理（10 分钟/天）健康大鼠和遭受由剂量（7.5 mg/kg）的 TMT 诱导的神经变性的大鼠，改变了 Na,K-ATP 酶催化亚基的表达，如以及这种酶在成年雄性 Wistar 大鼠额叶大脑皮层中的动力学特性。除了先前发表的对空间记忆的有益作用外，大鼠的日常治疗还伴随着额叶皮层钠稳态的改善。负责这一过程的关键系统 Na,K-ATPase 能够更好地利用能量底物 ATP。在大鼠中，对 TMT 诱导的神经变性的操作促进了酶的 α2 同工型的表达，这是胶质细胞的典型表现。在健康大鼠中，操作后 α3 亚基的表达增加，