Benzi G, Gorini A, Arnaboldi R, Ghigini B, Villa R
Institute of Pharmacology University of Pavia, Italy.
J Neurosci Res. 1993 Apr 15;34(6):654-63. doi: 10.1002/jnr.490340609.
Synaptosomal nonmitochondrial ATPases linked to the energy-utilizing systems were evaluated in cerebral cortex from normoxic rats and rats submitted to mild intermittent normobaric hypoxia [12 hr daily exposure to N2:O2 (90:10) mixture for 4 weeks]. The activities of Na+,K(+)-ATPase; high- and low-affinity Ca(2+)-ATPase; basal 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 either in normoxic rats or in hypoxic rats submitted to 4-week treatment with saline (controls) or a vasodilator agent (papaverine), an energy-metabolism interfering agent (theniloxazine), a calcium blocker (nicardipine), and a lipid-metabolism interfering agent (phosphatidylcholine) in order to define the plasticity and the selective changes in individual ATPases. In synaptosomes from rat cerebral cortex, the enzyme adaptation to the daily mild intermittent hypoxia for 4 weeks was characterized by an increase in the activity of Mg(2+)-ATPase, concomitant with a decrease in the activities of Na+,K(+)-ATPase, high-affinity Ca(2+)-ATPase, and Ca2+, Mg(2+)-ATPase. In hypoxic rats the enzyme adaptation to the 4-week treatment with phosphatidylcholine was characterized by an increase in Ca2+, Mg(2+)-ATPase activity and a decrease in Mg(2+)-ATPase activity. The action involves the enzymatic form located in the synaptic plasma membranes. In hypoxic rats the adaptation to the 4 week treatment with nicardipine was characterized by an increase in high-affinity Ca(2+)-ATPase activity, while the 4-week-treatment with theniloxazine induced an increase in Na+,K(+)-ATPase activity. The actions of both nicardipine and theniloxazine were related to the enzymatic forms located in the synaptic plasma membranes. The effects on the biophase induced by the sequential cycles of hypoxia/normoxia and the treatment with the various agents tested should also be related to the changes induced in the activity of some synaptosomal ATPases.
在常氧大鼠以及经历轻度间歇性常压缺氧的大鼠（每天暴露于N₂:O₂（90:10）混合气体中12小时，持续4周）的大脑皮层中，评估了与能量利用系统相关的突触体非线粒体ATP酶。在突触体及其亚组分，即突触体细胞膜和突触小泡中，测定了Na⁺,K⁺-ATP酶、高亲和力和低亲和力Ca²⁺-ATP酶、基础Mg²⁺-ATP酶以及Ca²⁺,Mg²⁺-ATP酶的活性。评估分别在常氧大鼠或经历4周盐水处理（对照组）或血管扩张剂（罂粟碱）、能量代谢干扰剂（噻尼嗪）、钙阻滞剂（尼卡地平）以及脂质代谢干扰剂（磷脂酰胆碱）处理的缺氧大鼠中进行，以确定各个ATP酶的可塑性和选择性变化。在大鼠大脑皮层的突触体中，酶对每日轻度间歇性缺氧4周的适应性表现为Mg²⁺-ATP酶活性增加，同时Na⁺,K⁺-ATP酶、高亲和力Ca²⁺-ATP酶以及Ca²⁺,Mg²⁺-ATP酶活性降低。在缺氧大鼠中，酶对磷脂酰胆碱4周处理的适应性表现为Ca²⁺,Mg²⁺-ATP酶活性增加而Mg²⁺-ATP酶活性降低。该作用涉及位于突触质膜中的酶形式。在缺氧大鼠中，酶对尼卡地平4周处理的适应性表现为高亲和力Ca²⁺-ATP酶活性增加，而噻尼嗪4周处理则诱导Na⁺,K⁺-ATP酶活性增加。尼卡地平和噻尼嗪的作用均与位于突触质膜中的酶形式有关。缺氧/常氧的连续循环以及所测试的各种药物处理对生物相的影响也应与某些突触体ATP酶活性的变化有关。
