Glutamate regulates actin-based motility in axonal filopodia

被引:120
|
作者
Chang, S
De Camilli, P
机构
[1] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06515 USA
[2] Yale Univ, Sch Med, Boyer Ctr Mol Med, Dept Cell Biol, New Haven, CT 06515 USA
关键词
D O I
10.1038/90489
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The dynamics of axonal arbors during synaptogenesis and their plasticity in the adult nervous system remain poorly understood. Axonal filopodia, which emerge from the shaft of axonal branches and contain small synaptic vesicle clusters, initiate synaptic formation. We found that the movement of axonal filopodia is strongly inhibited by the neurotransmitter glutamate. This inhibitory effect is local, requires extracellular Ca2+, and can be blocked by CNQX treatment but not by NMDA, implicating axonal AMPA/kainate glutamate receptors. Transport and exo-endocytic recycling of synaptic vesicle packages in filopodia are not affected. These results reveal that the effect of glutamate on axonal filopodia is similar to its previously described effect on dendritic spines. Our results raise the possibility that axonal ionotropic glutamate receptors are also involved in synaptic plasticity in the adult nervous system.
引用
收藏
页码:787 / 793
页数:7
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