TRANSIENT ISCHEMIA CAUSES A REDUCTION OF MG2+ BLOCKADE OF NMDA RECEPTORS

被引：36

作者：

HORI, N

CARPENTER, DO

机构：

[1] NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201

[2] SUNY ALBANY,SCH PUBL HLTH,ALBANY,NY 12201

来源：

NEUROSCIENCE LETTERS | 1994年 / 173卷 / 1-2期

关键词：

N-METHYL-D-ASPARTATE; VOLTAGE-DEPENDENCE; BLOCKADE; MAGNESIUM; ISCHEMIA; NEURONAL CELL DEATH;

D O I：

10.1016/0304-3940(94)90153-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

After transient ischemia, synaptic activation of neurons in CA1 results in an abnormally long depolarization. This is due to the appearance of an NMDA component which results from a decrease in the normal voltage-dependent blockade by Mg2+. The reduction of NMDA channel blockade is likely the cause of the hyperexcitability which follows transient ischemia and the subsequent delayed neuronal cell death, resulting from entry of calcium through hyperactive NMDA channels.

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页码：75 / 78

页数：4

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