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Synapsin II desynchronizes neurotransmitterrelease at inhibitory synapses by interactingwith presynaptic calcium channels

机译:Synapsin II通过与突触前钙通道相互作用,抑制抑制性突触中神经递质的释放

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摘要

In the central nervous system, most synapses show a fast mode of neurotransmitter releaseknown as synchronous release followed by a phase of asynchronous release, which extendsover tens of milliseconds to seconds. Synapsin II (SYN2) is a member of the multigenesynapsin family (SYN1/2/3) of synaptic vesicle phosphoproteins that modulate synaptictransmission and plasticity, and are mutated in epileptic patients. Here we report that inhibitorysynapses of the dentate gyrus of Syn II knockout mice display an upregulation ofsynchronous neurotransmitter release and a concomitant loss of delayed asynchronousrelease. Syn II promotes g-aminobutyric acid asynchronous release in a Ca2+-dependentmanner by a functional interaction with presynaptic Ca2+ channels, revealing a new role insynaptic transmission for synapsins.
机译:在中枢神经系统中,大多数突触显示出神经递质释放的快速模式,称为同步释放,其后是一个异步释放阶段,该阶段持续了数十毫秒到几秒钟。突触素II(SYN2)是突触小泡磷蛋白的多基因突触素家族(SYN1 / 2/3)的成员,可调节突触传递和可塑性,并在癫痫患者中发生突变。在这里我们报告说,Syn II基因敲除小鼠的齿状回的抑制性突触显示同步神经递质释放的上调和延迟异步释放的伴随损失。 Syn II通过与突触前Ca2 +通道的功能性相互作用促进Ca2 +依赖性方式中的g-氨基丁酸异步释放,从而揭示了突触传递蛋白在突触传递中的新作用。

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