Benzi G, Gorini A, Arnaboldi R, Ghigini B, Villa R F
Institute of Pharmacology, State University of Pavia, Italy.
J Neural Transm Suppl. 1994;44:159-71. doi: 10.1007/978-3-7091-9350-1_12.
The age-related alterations 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 synaptosomes and synaptosomal subfractions [namely, synaptosomal plasma membranes and synaptic vesicles] in the cerebral cortex from 3- and 24-month-old normoxic rats and rats subjected to either mild or severe chronic (four 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].
在来自3月龄和24月龄常氧大鼠以及经历轻度或重度慢性（四周）间歇性常压缺氧的大鼠的大脑皮质突触体和突触体亚组分（即突触体细胞膜和突触小泡）中，检测了与年龄相关的需能突触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。除高亲和性钙ATP酶外，衰老导致常氧大鼠的ATP酶活性降低。对轻度缺氧的适应性表现为：（i）3月龄大鼠中镁ATP酶活性增加，同时3月龄和24月龄大鼠的钠钾ATP酶和高亲和性钙ATP酶活性降低，以及（ii）3月龄大鼠中钙镁ATP酶活性降低。对慢性间歇性重度缺氧的适应性表现为：（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酶活性降低，以及（ii）仅24月龄大鼠的低亲和性钙ATP酶活性降低。对镁ATP酶活性的影响表现为位于突触细胞膜（参与ATP水解生成腺苷）的酶形式活性降低，同时位于突触小泡（参与递质如谷氨酸的周转）的酶形式活性增加。
