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首页> 外文期刊>Neuron >Excitatory and Inhibitory Neurons Utilize Different Ca 2+ Sensors and Sources to Regulate Spontaneous Release
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Excitatory and Inhibitory Neurons Utilize Different Ca 2+ Sensors and Sources to Regulate Spontaneous Release

机译：兴奋性和抑制性神经元利用不同的Ca 2+传感器和来源来调节自发释放

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Spontaneous neurotransmitter release (mini) is an important form of Ca2+-dependent synaptic transmission that occurs in the absence of action potentials. A molecular understanding of this process requires an identification of the underlying Ca2+sensors. Here, we address the roles of the relatively low-?and high-affinity Ca2+sensors, synapotagmin-1 (syt1) and Doc2α/β, respectively. We found that both syt1 and Doc2 regulate minis, but, surprisingly, their relative contributions depend on whether release was from excitatory or inhibitory neurons. Doc2α promoted glutamatergic minis, while Doc2β and syt1 both regulated GABAergic minis. We identified Ca2+ligand mutations in Doc2 that either disrupted or constitutively activated the regulation of minis. Finally, Ca2+entry via voltage-gated Ca2+channels triggered miniature GABA release by activating syt1, but had no effect on Doc2-driven minis. This work reveals an unexpected divergence in the regulation of spontaneous excitatory and inhibitory transmission in terms of both Ca2+sensors and sources.
机译：自发性神经递质释放（MINI）是一种重要形式的CA2 +依赖性突触传递，在没有动作电位的情况下发生。对该过程的分子理解需要识别底层CA2 +传感器。在这里，我们分别解决了相对低 - ？和高亲和力CA2 +传感器，Synapotagmin-1（Syt1）和Doc2α/β的角色。我们发现Syt1和Doc2调节Minis，但令人惊讶的是，它们的相对贡献取决于释放是否来自兴奋或抑制性神经元。 Doc2α促进了谷氨酸甲型迷你，而DOC2β和SYT1都调节了GABAergic Minis。我们鉴定了DOC2中的Ca2 +配体突变，其被破坏或组成型迷你调节。最后，通过电压门控Ca +通道进入CA2 +进入通过激活Syt1触发微型GABA释放，但对Doc2驱动的Mini没有影响。这项工作揭示了在CA2 +传感器和来源方面的自发兴奋性和抑制传输的调节方面存在意外分歧。

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