Benzi G, Gorini A, Arnaboldi R, Ghigini B, Villa R F
Institute of Pharmacology, State University of Pavia, Italy.
Neurochem Int. 1994 Jul;25(1):61-7. doi: 10.1016/0197-0186(94)90054-x.
In synaptosomes and synaptosomal subfractions (namely, synaptosomal plasma membranes and synaptic vesicles) the age-related alteration in the plasticity of synaptic energy-requiring ATPases (Na+, K(+)-ATPase, low- and high-affinity Ca(2+)-ATPase, Mg(2+)-ATPase and Ca2+, Mg(2+)-ATPase) were assayed in the cerebral cortex from 3- and 24-month-old normoxic rats and rats subjected to either mild or severe chronic (4 weeks) intermittent normobaric hypoxia. With the exception of the high-affinity Ca(2+)-ATPase, aging induced a decrease in the ATPase activities from normoxic rats. The adaptation to mild hypoxia was characterized by an increase in the activity of Mg(2+)-ATPase in 3-month-old rats, concomitant with a decrease in the activities of: (i) Na+,K(+)-ATPase and high-affinity Ca(2+)-ATPase in both 3- and 24-month-old rats; and (ii) Ca2+,Mg(2+)-ATPase in 3-month-old ones. The adaptation to chronic intermittent severe hypoxia was characterized by a decrease in the activities of: (i) Na+,K(+)-ATPase, Ca2+,Mg(2+)-ATPase and high-affinity Ca(2+)-ATPase in both 3- and 24-month-old rats and (ii) low-affinity Ca(2+)-ATPase only in 24-month-old ones. The effect on Mg(2+)-ATPase activity was characterized by a decrease in the activity of the enzymatic form located in the synaptic plasma membranes (involved in ATP hydrolysis to adenosine production), concomitant with an increase in the activity of the form located in the synaptic vesicles (involved in the turnover of transmitters, e.g., glutamate).
在突触体和突触体亚组分（即突触体质膜和突触小泡）中，对3月龄和24月龄常氧大鼠以及经历轻度或重度慢性（4周）间歇性常压缺氧的大鼠的大脑皮质中，与年龄相关的突触能量依赖性ATP酶（钠钾ATP酶、低亲和性和高亲和性钙ATP酶、镁ATP酶以及钙镁ATP酶）可塑性变化进行了测定。除高亲和性钙ATP酶外，衰老导致常氧大鼠的ATP酶活性降低。轻度缺氧适应的特征是3月龄大鼠的镁ATP酶活性增加，同时伴有以下酶活性降低：（i）3月龄和24月龄大鼠的钠钾ATP酶和高亲和性钙ATP酶；（ii）3月龄大鼠的钙镁ATP酶。慢性间歇性重度缺氧适应的特征是以下酶活性降低：（i）3月龄和24月龄大鼠的钠钾ATP酶、钙镁ATP酶和高亲和性钙ATP酶；（ii）仅24月龄大鼠的低亲和性钙ATP酶。对镁ATP酶活性的影响表现为位于突触质膜的酶形式（参与ATP水解生成腺苷）的活性降低，同时位于突触小泡的酶形式（参与递质如谷氨酸的周转）的活性增加。
