Glutamate regulates actin-based motility in axonal filopodia
Glutamate regulates actin-based motility in axonal filopodia
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DOI：
10.1038/90489
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发表时间：
2001-08-01
影响因子：
25
通讯作者：
De Camilli, P
中科院分区：
文献类型：
--
作者：
Chang, S;De Camilli, P
在成年神经系统中，突触发生过程中轴突的动力学及其可塑性仍然知之甚少。轴突丝足，从轴突分支的轴中出现，包含小的突触囊泡簇，启动突触的形成。我们发现，轴突丝状伪足的运动受到神经递质谷氨酸的强烈抑制。这种抑制作用是局部的，需要细胞外Ca 2+，并且可以被CNQX处理阻断，但不能被NMDA阻断，涉及轴突AMPA/红藻氨酸谷氨酸受体。在丝状伪足中突触囊泡包的运输和外吞-内吞再循环不受影响。这些结果表明，谷氨酸对轴突丝状伪足的作用类似于其先前描述的对树突棘的作用。我们的研究结果提出了轴突离子型谷氨酸受体也参与成人神经系统突触可塑性的可能性。
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.