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Synapsin II desynchronizes neurotransmitter release at inhibitory synapses by interacting with presynaptic calcium channels

机译:Synapsin II通过与突触前钙通道相互作用使抑制性突触中的神经递质释放失同步

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摘要

In the central nervous system, most synapses show a fast mode of neurotransmitter release known as synchronous release followed by a phase of asynchronous release, which extends over tens of milliseconds to seconds. Synapsin II (SYN2) is a member of the multigene synapsin family (SYN1/2/3) of synaptic vesicle phosphoproteins that modulate synaptic transmission and plasticity, and are mutated in epileptic patients. Here we report that inhibitory synapses of the dentate gyrus of Syn II knockout mice display an upregulation of synchronous neurotransmitter release and a concomitant loss of delayed asynchronous release. Syn II promotes γ-aminobutyric acid asynchronous release in a Ca2+-dependent manner by a functional interaction with presynaptic Ca2+ channels, revealing a new role in synaptic 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,该阶段持续数十毫秒至数秒。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Ca 2 + 通道的功能相互作用,以Ca 2 + 依赖的方式促进γ-氨基丁酸异步释放,从而揭示了突触传递中的新作用。突触蛋白。

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