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谷氨酸诱导的突触后致密物的瞬时修饰。

Glutamate-induced transient modification of the postsynaptic density.

作者信息

Dosemeci A, Tao-Cheng J H, Vinade L, Winters C A, Pozzo-Miller L, Reese T S

机构信息

Marine Biological Laboratories, Woods Hole, MA 02543, USA.

出版信息

Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10428-32. doi: 10.1073/pnas.181336998. Epub 2001 Aug 21.

Abstract

Depolarization of rat hippocampal neurons with a high concentration of external potassium induces a thickening of postsynaptic densities (PSDs) within 1.5-3 min. After high-potassium treatment, PSDs thicken 2.1-fold in cultured neurons and 1.4-fold in hippocampal slices compared with their respective controls. Thin-section immunoelectron microscopy of hippocampal cultures indicates that at least part of the observed thickening of PSDs can be accounted for by an accumulation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) on their cytoplasmic faces. Indeed, PSD-associated gold label for CaMKII increases 5-fold after depolarization with potassium. The effects of high-potassium treatment on the composition and structure of the PSDs are mimicked by direct application of glutamate. In cultures, glutamate-induced thickening of PSDs and the accumulation of CaMKII on PSDs are reversed within 5 min of removal of glutamate and Ca(2+) from the extracellular medium. These results suggest that PSDs are dynamic structures whose thickness and composition are subject to rapid and transient changes during synaptic activity.

摘要

用高浓度的细胞外钾使大鼠海马神经元去极化会在1.5 - 3分钟内诱导突触后致密物(PSD)增厚。与各自的对照相比,高钾处理后,培养神经元中的PSD增厚2.1倍,海马切片中的PSD增厚1.4倍。海马培养物的超薄切片免疫电子显微镜检查表明,观察到的PSD增厚至少部分可归因于Ca(2 +)/钙调蛋白依赖性蛋白激酶II(CaMKII)在其细胞质面上的积累。实际上,去极化后,PSD相关的CaMKII金标记增加5倍。直接应用谷氨酸可模拟高钾处理对PSD组成和结构的影响。在培养物中,谷氨酸诱导的PSD增厚和CaMKII在PSD上的积累在从细胞外培养基中去除谷氨酸和Ca(2 +)后5分钟内逆转。这些结果表明,PSD是动态结构,其厚度和组成在突触活动期间会发生快速和短暂的变化。

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Glutamate-induced transient modification of the postsynaptic density.谷氨酸诱导的突触后致密物的瞬时修饰。
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10428-32. doi: 10.1073/pnas.181336998. Epub 2001 Aug 21.

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