首页> 美国卫生研究院文献>The Journal of Neuroscience >Postsynaptic Calcium/Calmodulin-Dependent Protein Kinase II Is Required to Limit Elaboration of Presynaptic and Postsynaptic Neuronal Arbors
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Postsynaptic Calcium/Calmodulin-Dependent Protein Kinase II Is Required to Limit Elaboration of Presynaptic and Postsynaptic Neuronal Arbors

机译:突触后钙/钙调蛋白依赖性蛋白激酶II是必需的以限制精细化的突触前和突触后神经元乔木。

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摘要

Neuronal dendritic and axonal arbors grow to a characteristic size and then stabilize their structures. Activity-dependent stop-growing signals may limit neuronal process elaboration. We tested whether endogenous calcium/calmodulin-dependent protein kinase II (CaMKII) activity in postsynaptic optic tectal cells is required to restrict the elaboration of neuronal processes in the Xenopus tadpole retinotectal projection. Optic tectal cells were infected with vaccinia viruses that express CaMKII-specific inhibitory peptides. In vivo time-lapse imaging revealed that expression of CaMKII inhibitors blocked the growth restriction that normally occurs during maturation of tectal cell dendritic arbors. Postsynaptic CaMKII inhibition also increased the growth of presynaptic retinotectal axon arbors. The results indicate that endogenous postsynaptic CaMKII activity is required to limit the growth of presynaptic and postsynaptic arbor structures in vivo.
机译:神经元树突状和轴突的树突生长到特定大小,然后稳定其结构。依赖活动的停止生长信号可能会限制神经元过程的形成。我们测试了是否需要限制突触后optic盖中神经元过程的精细化,是否需要突触后视神经顶细胞中的内源性钙/钙调蛋白依赖性蛋白激酶II(CaMKII)活性。用表达CaMKII特异性抑制肽的牛痘病毒感染视神经细胞。体内延时成像显示,CaMKII抑制剂的表达阻断了在顶盖细胞树突状树突成熟期间通常发生的生长限制。突触后CaMKII抑制作用也增加了突触前视网膜-视神经轴突轴突的生长。结果表明,需要内源性突触后CaMKII活性来限制体内突触前和突触后乔木结构的生长。

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