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首页> 美国卫生研究院文献>The Journal of Neuroscience >Stabilization of Spontaneous Neurotransmitter Release at Ribbon Synapses by Ribbon-Specific Subtypes of Complexin
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Stabilization of Spontaneous Neurotransmitter Release at Ribbon Synapses by Ribbon-Specific Subtypes of Complexin

机译：复杂功能区的功能区特定亚型稳定功能区突触自发神经递质的释放。

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Ribbon synapses of tonically releasing sensory neurons must provide a large pool of releasable vesicles for sustained release, while minimizing spontaneous release in the absence of stimulation. Complexins are presynaptic proteins that may accomplish this dual task at conventional synapses by interacting with the molecular machinery of synaptic vesicle fusion at the active zone to retard spontaneous vesicle exocytosis yet facilitate release evoked by depolarization. However, ribbon synapses of photoreceptor cells and bipolar neurons in the retina express distinct complexin subtypes, perhaps reflecting the special requirements of these synapses for tonic release. To investigate the role of ribbon-specific complexins in transmitter release, we combined presynaptic voltage clamp, fluorescence imaging, electron microscopy, and behavioral assays of photoreceptive function in zebrafish. Acute interference with complexin function using a peptide derived from the SNARE-binding domain increased spontaneous synaptic vesicle fusion at ribbon synapses of retinal bipolar neurons without affecting release triggered by depolarization. Knockdown of complexin by injection of an antisense morpholino into zebrafish embryos prevented photoreceptor-driven migration of pigment in skin melanophores and caused the pigment distribution to remain in the dark-adapted state even when embryos were exposed to light. This suggests that loss of complexin function elevated spontaneous release in illuminated photoreceptors sufficiently to mimic the higher release rate normally associated with darkness, thus interfering with visual signaling. We conclude that visual system-specific complexins are required for proper illumination-dependent modulation of the rate of neurotransmitter release at visual system ribbon synapses.
机译：调性释放的感觉神经元的带状突触必须提供大量可释放的囊泡以持续释放，同时在没有刺激的情况下最大程度地减少自发释放。复杂蛋白是突触前蛋白，可以通过在活性区与突触小泡融合的分子机制相互作用来阻止自发性小泡胞吐作用，同时促进去极化引起的释放，从而在常规突触中完成此双重任务。然而，视网膜中感光细胞和双极神经元的带状突触表达不同的复合蛋白亚型，这可能反映了这些突触对滋补释放的特殊要求。为了研究带状特定复合物在递质释放中的作用，我们结合了突触前电压钳，荧光成像，电子显微镜和斑马鱼光感受功能的行为分析。使用源自SNARE结合域的肽对复合蛋白功能的急性干扰会增加视网膜双极神经元的带状突触处的自发突触囊泡融合，而不影响去极化触发的释放。通过将反义吗啉代注射到斑马鱼胚胎中来抑制复合蛋白，可以防止光感受器驱动的色素在皮肤黑素细胞中迁移，并且即使在胚胎暴露于光线的情况下，色素分布仍保持在暗适应状态。这表明，复杂蛋白功能的丧失充分提高了受照感光体的自发释放，足以模仿通常与黑暗有关的更高释放速率，从而干扰了视觉信号。我们得出结论，视觉系统特定的复合蛋白是视觉系统功能区突触时神经递质释放速率的适当照度依赖性调节所必需的。

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