The use of antioxidants to prevent glutamate-induced derangement of calcium ion metabolism in rat cerebral cortex synaptosomes

被引：29

作者：

Avrova N.F. ^{[1
]}

Shestak K.I. ^{[1
]}

Zakharova I.O. ^{[1
]}

Sokolova T.V. ^{[1
]}

Tyurina Yu.Yu. ^{[1
]}

Tyurin V.A. ^{[1
]}

机构：

[1] I. M. Sechenov Inst. Evol. Physiol., Russian Academy of Sciences, 44 M. Torez Prospekt

来源：

Neuroscience and Behavioral Physiology | 2000年 / 30卷 / 5期

基金：

俄罗斯基础研究基金会;

关键词：

Antioxidants; Brain synaptosomes; Calcium ions; Glutamate; GM1; ganglioside;

D O I：

10.1007/BF02462611

中图分类号：

学科分类号：

摘要：

Glutamate is shown to induce increases in intracellular Ca2+ concentrations ([Ca2+](i)), increases in 45Ca2+ influx, decreases in the activity of Na+,K+-ATPase activity, and activation of the Na+/Ca2+ exchanger in rat cerebral cortex synaptosomes. NMDA receptor antagonists virtually prevented these effects. Preincubation of synaptosomes with α-tocopherol, superoxide dismutase, and ganglioside GM1 normalized [Ca2+](i), 45Ca2+ influx, and Na+,K+-ATPase activity in rat cerebral cortex synaptosomes exposed to glutamate. Glutamate and GM1 activated the Na+/K+ exchanger, and their effects were additive. Calcium ions entering cerebral cortex nerve cells via NMDA receptors during exposure to high glutamate concentrations appeared to be only the trigger for the processes activating free-radical reactions. Activation of these reactions led to increases in Ca2+ influx into cells, decreases in Na+,K+-ATPase activity, and significant increases in [Ca2+](i), though this could be prevented by antioxidants and gangliosides.

引用

页码：535 / 541

页数：6

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