A role for primary cilia in glutamatergic synaptic integration of adult-born neurons

被引:143
作者
Kumamoto, Natsuko [1 ]
Gu, Yan [1 ]
Wang, Jia [1 ]
Janoschka, Stephen [1 ,2 ]
Takemaru, Ken-Ichi [3 ]
Levine, Joel [1 ]
Ge, Shaoyu [1 ]
机构
[1] SUNY Stony Brook, Dept Neurobiol & Behav, Stony Brook, NY 11794 USA
[2] SUNY Stony Brook, Program Neurosci, Stony Brook, NY 11794 USA
[3] SUNY Stony Brook, Dept Pharmacol Sci, Stony Brook, NY 11794 USA
基金
美国国家卫生研究院;
关键词
NEWLY GENERATED NEURONS; BETA-CATENIN; HIPPOCAMPAL NEUROGENESIS; DENTATE GYRUS; PROGENITOR POOL; BRAIN; MORPHOGENESIS; DISEASE; MALFORMATION; MECHANISMS;
D O I
10.1038/nn.3042
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The sequential synaptic integration of adult-born neurons has been widely examined in rodents, but the mechanisms regulating the integration remain largely unknown. The primary cilium, a microtubule-based signaling center, is essential for vertebrate development, including the development of the CNS. We examined the assembly and function of the primary cilium in the synaptic integration of adult-born mouse hippocampal neurons. Primary cilia were absent in young adult-born neurons, but assembled precisely at the stage when newborn neurons approach their final destination, further extend dendrites and form synapses with entorhinal cortical projections. Conditional deletion of cilia from adult-born neurons induced severe defects in dendritic refinement and synapse formation. Deletion of primary cilia led to enhanced Wnt and beta-catenin signaling, which may account for these developmental defects. Taken together, our findings identify the assembly of primary cilia as a critical regulatory event in the dendritic refinement and synaptic integration of adult-born neurons.
引用
收藏
页码:399 / U79
页数:8
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