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首页> 外文期刊>Neuron >Transient Confinement of Ca(V)2.1 Ca2+-Channel Splice Variants Shapes Synaptic Short-Term Plasticity
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Transient Confinement of Ca(V)2.1 Ca2+-Channel Splice Variants Shapes Synaptic Short-Term Plasticity

机译：CA（v）2.1 CA2 + -Channel剪接变体的瞬态限制形状突触短期可塑性

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摘要

The precision and reliability of synaptic information transfer depend on the molecular organization of voltage-gated calcium channels (VGCCs) within the presynaptic membrane. Alternative splicing of exon 47 affects the C-terminal structure of VGCCs and their affinity to intracellular partners and synaptic vesicles (SVs). We show that hippocampal synapses expressing VGCCs either with exon 47 (Ca(V)2.1(+47)) or without (Ca(V)2.1(Delta 47)) differ in release probability and short-term plasticity. Tracking single channels revealed transient visits (similar to 100 ms) of presynaptic VGCCs in nanodomains (similar to 80 nm) that were controlled by neuronal network activity. Surprisingly, despite harboring prominent binding sites to scaffold proteins, CaV2.1(+47) persistently displayed higher mobility within nanodomains. Synaptic accumulation of Ca(V)2.1 was accomplished by optogenetic clustering, but only CaV2.1(+47) increased transmitter release and enhanced synaptic short-term depression. We propose that exon 47-related alternative splicing of Ca(V)2.1 channels controls synapse-specific release properties at the level of channel mobility-dependent coupling between VGCCs and SVs.
机译：突触信息转移的精度和可靠性取决于突触膜内的电压门控钙通道（VGCC）的分子组织。外显子47的替代剪接影响VGCC的C末端结构及其对细胞内伴侣和突触囊泡（SV）的亲和力。我们表明，用外显子47（Ca（v）2.1（+ 47））或没有（Ca（V）2.1（Δ47））的释放概率和短期可塑性不同。跟踪单个通道显示通过神经网络活动控制的纳米型（类似于80nm）的瞬态访问（类似于100 ms）的突触前VGCC。令人惊讶的是，尽管含有突出的结合位点到支架蛋白，Cav2.1（+ 47）持续地显示在纳米染色型内的更高迁移率。 Ca（v）2.1的突触积累是通过光学聚类完成的，但只有CAV2.1（+ 47）增加发射器释放和增强突触短期抑郁症。我们提出了外显子47相关的CA（v）2.1信道的替代剪接在VGCC和SV之间的信道移动依赖性耦合水平下控制突触特定的释放属性。

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  • 来源
    《Neuron》 |2019年第1期|共26页
  • 作者

    Heck Jennifer; Parutto Pierre; Ciuraszkiewicz Anna; Bikbaev Arthur; Freund Romy; Mitloehner Jessica; Andres-Alonso Maria; Fejtova Anna; Holcman David; Heine Martin;

  • 作者单位

    Leibniz Inst Neurobiol Res Grp Mol Physiol Brenneckestr 6 D-39118 Magdeburg Germany;

    Ecole Normale Super IBENS Grp Appl Math &

    Computat Biol Paris France;

    Leibniz Inst Neurobiol Res Grp Mol Physiol Brenneckestr 6 D-39118 Magdeburg Germany;

    Leibniz Inst Neurobiol Res Grp Mol Physiol Brenneckestr 6 D-39118 Magdeburg Germany;

    Leibniz Inst Neurobiol Res Grp Mol Physiol Brenneckestr 6 D-39118 Magdeburg Germany;

    Leibniz Inst Neurobiol Dept Neurochem &

    Mol Biol Brenneckestr 6 D-39118 Magdeburg Germany;

    Leibniz Inst Neurobiol Res Grp Presynapt Plast Brenneckestr 6 D-39118 Magdeburg Germany;

    Otto von Guericke Univ CBBS D-39106 Magdeburg Germany;

    Ecole Normale Super IBENS Grp Appl Math &

    Computat Biol Paris France;

    Leibniz Inst Neurobiol Res Grp Mol Physiol Brenneckestr 6 D-39118 Magdeburg Germany;

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  • 正文语种 eng
  • 中图分类 神经病学;
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