SYNAPTOSOMAL NONMITOCHONDRIAL ATPASE ACTIVITIES - AGE-RELATED ALTERATIONS BY CHRONIC NORMOBARIC INTERMITTENT HYPOXIA

SYNAPTOSOMAL NONMITOCHONDRIAL ATPASE ACTIVITIES - AGE-RELATED ALTERATIONS BY CHRONIC NORMOBARIC INTERMITTENT HYPOXIA
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DOI:
10.1016/0197-0186(94)90054-x
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发表时间:
1994-07-01
影响因子:
4.2
通讯作者:
VILLA, RF
VILLA, RF
中科院分区:
医学3区
文献类型:
--
作者:
BENZI, G;GORINI, A;VILLA, RF

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在突触体和突触体亚组分中(即突触体质膜和突触小泡)突触能量需求ATP酶可塑性的年龄相关改变(Na+,K+-ATP酶,低-和高-amnity Ca 2 +-ATP酶:Mg ~(2+)-ATP酶和Ca ~(2+),测定了3月龄和24月龄常氧大鼠和轻度或重度慢性(4周)间歇性常压缺氧除高亲和力的Ca ~(2+)-ATP酶外,衰老诱导常氧大鼠ATP酶活性下降。轻度低氧适应的特点是3月龄大鼠Mg 2 +-ATP酶活性升高,同时伴有3月龄和24月龄大鼠Na+,K+-ATP酶和高亲和力Ca 2 +-ATP酶活性降低,3月龄大鼠Ca 2+,Mg 2 +-ATP酶活性降低。慢性间歇性低氧适应的特点是:(i)3月龄和24月龄大鼠的Na+,K+-ATP酶、Ca ~(2+),Mg ~(2+)-ATP酶和高亲和力Ca ~(2+)-ATP酶活性均下降;(ii)低亲和力Ca ~(2+)-ATP酶仅在24月龄大鼠下降。对Mg 2 +-ATP酶活性的影响的特征在于位于突触质膜中的酶形式(参与ATP水解产生腺苷)的活性降低,伴随着位于突触囊泡中的形式(参与递质的周转,例如,谷氨酸盐)。
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-amnity Ca2+-ATPase: Mg2+-ATPase and Ca2+, Mg2+-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 Ca2+- 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 Mg2+-ATPase in 3-month-old rats, concomitant with a decrease in the activities of: (i) Na+, K+-ATPase and high-affinity Ca2+-ATPase in both 3- and 24-month-old rats; and (ii) Ca2+, Mg2+-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+, Mg2+-ATPase and high-affinity Ca2+-ATPase in both 3- and 24-month-old rats and (ii) low-affinity Ca2+-ATPase only in 24-month-old ones. The effect on Mg2+-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).