Regulation of neurotransmitter release by synapsin III
Regulation of neurotransmitter release by synapsin III
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DOI：
10.1523/jneurosci.22-11-04372.2002
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发表时间：
2002-06-01
影响因子：
5.3
通讯作者：
Greengard, P
中科院分区：
文献类型：
--
作者：
Feng, J;Chi, P;Greengard, P
突触素III是突触蛋白家族的最新成员，突触蛋白是一组突触囊泡蛋白，它们在神经递质释放和神经突生长中起重要作用。在这里，通过对突触素III敲除小鼠的产生和分析，我们证明了突触素III以与突触素I或Synapsin II不同的方式调节神经递质释放。在缺乏突触素III的小鼠中，突触囊泡的回收池的大小增加，并减少了突触抑制。融合每个动作电位的囊泡的数量在突触III敲除和野生型小鼠之间相似，并且EPSC的量子含量没有变化。但是，IPSC在缺陷型神经元中大大降低。与野生型同窝鼠相比，突触前末端的突触囊泡的密度和分布似乎没有不同。除了神经递质释放的变化外，我们还观察到来自突触素III敲除小鼠的培养的海马神经元中轴突生长的特异性延迟。我们的数据表明，突触素III在早期轴突生长和突触囊泡运输的调节中都起着独特的作用。
Synapsin III is the most recently identified member of the synapsin family, a group of synaptic vesicle proteins that play essential roles in neurotransmitter release and neurite outgrowth. Here, through the generation and analysis of synapsin III knock-out mice, we demonstrate that synapsin III regulates neurotransmitter release in a manner that is distinct from that of synapsin I or synapsin II. In mice lacking synapsin III, the size of the recycling pool of synaptic vesicles was increased, and synaptic depression was reduced. The number of vesicles that fuse per action potential was similar between synapsin III knock-out and wild-type mice, and there was no change in the quantal content of EPSCs; however, IPSCs were greatly reduced in synapsin III-deficient neurons. The density and distribution of synaptic vesicles in presynaptic terminals did not appear to be different in synapsin III knock-out mice in comparison to wild-type littermates. In addition to the changes in neurotransmitter release, we observed a specific delay in axon outgrowth in cultured hippocampal neurons from synapsin III knock-out mice. Our data indicate that synapsin III plays unique roles both in early axon outgrowth and in the regulation of synaptic vesicle trafficking.