Glutamate-induced transient modification of the postsynaptic density
Glutamate-induced transient modification of the postsynaptic density
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DOI：
10.1073/pnas.181336998
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发表时间：
2001-08-28
影响因子：
11.1
通讯作者：
Reese, TS
中科院分区：
文献类型：
--
作者：
Dosemeci, A;Tao-Cheng, JH;Reese, TS
高浓度外源性钾使大鼠海马神经元去极化，在1.5-3分钟内引起突触后密度(PSD)增厚。高钾处理后，PSD在培养神经元中的厚度是各自对照的2.1倍，在海马片中是各自对照的1.4倍。海马区培养物的薄片免疫电子显微镜显示，至少部分观察到的PSD增厚可归因于其细胞质表面钙/钙调蛋白依赖的蛋白激酶II(CaMKII)的积聚。事实上，PSD相关的CaMKII的金标记物在钾去极化后增加了5倍。通过直接应用谷氨酸来模拟高钾处理对PSD组成和结构的影响。在培养中，谷氨酸引起的PSD增厚和CaMKII在PSD上的积聚在细胞外培养液中去除谷氨酸和钙离子后5分钟内被逆转。这些结果表明，PSD是一种动态结构，其厚度和成分在突触活动过程中会发生快速和瞬时的变化。
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 Ca2+/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 Ca2+ 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.