Benzi G, Gorini A, Ghigini B, Arnaboldi R, Villa R F
Institute of Pharmacology-State University of Pavia, Italy.
Neurochem Res. 1994 Apr;19(4):517-24. doi: 10.1007/BF00967332.
The plasticity of synaptosomal non-mitochondrial ATPases was evaluated in cerebral cortex from 3-month-old normoxic rats and rats subjected to either mild or severe intermittent normobaric hypoxia [12 hr daily exposure to N2:O2 (90:10 or 91.5:8.5) for four weeks]. The activities of Na+, K(+)-ATPase, low- and high-affinity Ca(2+)-ATPase, Mg(2+)-ATPase, and Ca2+,Mg(2+)-ATPase were assayed in synaptosomes and synaptosomal subfractions, namely synaptosomal plasma membranes and synaptic vesicles. The evaluations were performed after a 4-week treatment with saline (controls) or alpha-adrenergic agents (delta-yohimbine, clonidine), a vasodilator compound (papaverine), and an oxygen-partial pressure increasing agent (almitrine). These treatments differently changed the adaptation to chronic intermittent hypoxia characterized by a decrease in the activity of Na+,K(+)-ATPase, Ca2+,Mg(2+)-ATPase, and high-affinity Ca(2+)-ATPase, concomitant with a modification in the activity of Mg(2+)-ATPase supported in a different way by the enzymatic forms located into the synaptosomal plasma membranes and synaptic vesicles.
在3月龄常氧大鼠以及经历轻度或重度间歇性常压缺氧的大鼠（每天暴露于N2:O2（90:10或91.5:8.5）12小时，持续四周）的大脑皮层中评估了突触体非线粒体ATP酶的可塑性。在突触体及其亚组分（即突触体质膜和突触小泡）中测定了Na +、K(+)-ATP酶、低亲和力和高亲和力Ca(2+)-ATP酶、Mg(2+)-ATP酶以及Ca2+、Mg(2+)-ATP酶的活性。在用生理盐水（对照组）或α-肾上腺素能药物（δ-育亨宾、可乐定）、一种血管扩张剂化合物（罂粟碱）以及一种氧分压升高剂（阿米三嗪）进行4周治疗后进行了评估。这些治疗以不同方式改变了对慢性间歇性缺氧的适应性，其特征为Na +、K(+)-ATP酶、Ca2+、Mg(2+)-ATP酶和高亲和力Ca(2+)-ATP酶的活性降低，同时突触体质膜和突触小泡中不同酶形式所支持的Mg(2+)-ATP酶活性发生改变。
