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体内由钙/钙调蛋白依赖性蛋白激酶II实现的树突状分支结构稳定化。

Stabilization of dendritic arbor structure in vivo by CaMKII.

作者信息

Wu G Y, Cline H T

机构信息

Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.

出版信息

Science. 1998 Jan 9;279(5348):222-6. doi: 10.1126/science.279.5348.222.

Abstract

Calcium-calmodulin-dependent protein kinase II (CaMKII) promotes the maturation of retinotectal glutamatergic synapses in Xenopus. Whether CaMKII activity also controls morphological maturation of optic tectal neurons was tested using in vivo time-lapse imaging of single neurons over periods of up to 5 days. Dendritic arbor elaboration slows with maturation, in correlation with the onset of CaMKII expression. Elevating CaMKII activity in young neurons by viral expression of constitutively active CaMKII slowed dendritic growth to a rate comparable to that of mature neurons. CaMKII overexpression stabilized dendritic structure in more mature neurons, whereas CaMKII inhibition increased their dendritic growth. Thus, endogenous CaMKII activity limits dendritic growth and stabilizes dendrites, and it may act as an activity-dependent mediator of neuronal maturation.

摘要

钙调蛋白依赖性蛋白激酶II(CaMKII)促进非洲爪蟾视网膜顶盖谷氨酸能突触的成熟。通过对单个神经元进行长达5天的体内延时成像,测试了CaMKII活性是否也控制视顶盖神经元的形态成熟。随着成熟,树突分支的细化减缓,这与CaMKII表达的开始相关。通过组成型活性CaMKII的病毒表达提高年轻神经元中的CaMKII活性,可使树突生长减缓至与成熟神经元相当的速率。CaMKII的过表达使更成熟神经元中的树突结构稳定,而CaMKII的抑制则增加了它们的树突生长。因此,内源性CaMKII活性限制树突生长并稳定树突,它可能作为神经元成熟的活性依赖性介质发挥作用。

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