Department of Biochemistry, Faculty of Medicine, Tartu University, Ravila 19, Tartu, Estonia.
Neurochem Res. 2010 May;35(5):688-92. doi: 10.1007/s11064-009-0119-1. Epub 2010 Jan 8.
Previously we have shown that the temperature dependence of the sodium pump (Na(+),K(+)-ATPase) is altered under different neuropathological conditions. In this study we compared temperature dependence of the Na(+),K(+)-ATPase in the fronto-parietal cortex of CCK(2) receptor-deficient (homo- and heterozygous) and normal (wild-type) mice. The Arrhenius plot for Na(+),K(+)-ATPase from wild-type brain is non-linear with a breakpoint at 20.3 +/- 0.4 degrees C. In case of the brain cell membrane of CCK(2) receptor-deficient mice (homo- and heterozygous) the breakpoint on Arrhenius plot was detected at 26.0 +/- 1.1 degrees C and 25.4 +/- 0.4 degrees C, respectively. The shift of the breakpoint on the Arrhenius plot established in CCK(2) receptor-deficiency as well as in case of some other pathological conditions confirms that such kind of alteration in the Na(+),K(+)-ATPase temperature dependence is likely related to the homeostatic adjustment of altered function of the sodium pump.
先前,我们已经表明在不同的神经病理学条件下,钠泵(Na(+),K(+)-ATPase)的温度依赖性会发生改变。在这项研究中,我们比较了 CCK(2)受体缺失(同型和杂合)和正常(野生型)小鼠的额顶皮质中的 Na(+),K(+)-ATPase 的温度依赖性。野生型脑组织中 Na(+),K(+)-ATPase 的 Arrhenius 图是非线性的,断点在 20.3 +/- 0.4 摄氏度。在 CCK(2)受体缺失的小鼠(同型和杂合)的脑细胞膜中,Arrhenius 图的断点分别检测到在 26.0 +/- 1.1 摄氏度和 25.4 +/- 0.4 摄氏度。在 CCK(2)受体缺失以及其他一些病理条件下建立的 Arrhenius 图上断点的移动证实,这种 Na(+),K(+)-ATPase 温度依赖性的改变可能与钠泵功能改变的稳态调节有关。