学习与记忆机制研究进展

被引：7

作者：

周星娟

凌树才

机构：

[1] 浙江大学人体解剖与组织胚胎学

来源：

国际病理科学与临床杂志 | 2008年 / 02期

关键词：

长时程增强; 学习记忆; 受体; 蛋白激酶; 基因表达;

D O I：

暂无

中图分类号：

R338 [神经生理学];

学科分类号：

0710 ; 071006 ;

摘要：

学习与记忆是动物最具特色的高级神经活动之一,长时程增强(LTP)被认为是与学习记忆有关的神经元可塑性的理想模型,其分子机制涉及一个信号转导级联反应———谷氨酸释放、N-甲基-D-天(门)冬氨酸(N-Methyl-D-aspartic acid,NMDA)谷氨酸受体激活、Ca2+通道和Ca2+/钙调蛋白依赖性蛋白激酶(Ca2+/calmodulin-de-pendent protein kinases,CaM激酶)Ⅱ、Ⅳ和丝裂原蛋白激酶(mitogen-activated protein kinase,MAPK)激活。最后,CaM激酶Ⅱ使α-氨基羟甲基恶唑丙酸(α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid,AMPA)谷氨酸受体磷酸化而激活,引起突触后神经元Ca2+内流增加。CaM激酶Ⅳ和MAPK通过刺激基因表达促使环磷腺苷反应元件结合蛋白(cyclic AMP response element binding protein,CREB)磷酸化水平升高,c-fos表达增加。

引用

页码：138 / 141

页数：4

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