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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Differential Dependence Of Phasic Transmitter Release On Synaptotagmin 1 At Gabaergic And Glutamatergic Hippocampal Synapses
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Differential Dependence Of Phasic Transmitter Release On Synaptotagmin 1 At Gabaergic And Glutamatergic Hippocampal Synapses

机译：Gabaergic和Glutamatergic海马突触中突触释放素1的相位释放释放的差异性依赖性

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摘要

Previous studies revealed that synaptotagmin 1 is the major Ca~(2+) sensor for fast synchronous transmitter release at excitatory synapses. However, the molecular identity of the Ca~(2+) sensor at hippocampal inhibitory synapses has not been determined. To address the functional role of synaptotagmin 1 at identified inhibitory terminals, we made paired recordings from synaptically connected basket cells (BCs) and granule cells (GCs) in the dentate gyrus in organotypic slice cultures from wild-type and synaptotagmin 1-deficient mice. As expected, genetic elimination of synaptotagmin 1 abolished synchronous transmitter release at excitatory GC-BC synapses. However, synchronous release at inhibitory BC-GC synapses was maintained. Quantitative analysis revealed that elimination of synaptotagmin 1 reduced release probability and depression but maintained the synchrony of transmitter release at BC-GC synapses. Elimination of synaptotagmin 1 also increased the frequency of both miniature excitatory postsynaptic currents (measured in BCs) and miniature inhibitory postsynaptic currents (recorded in GCs), consistent with a clamping function of synaptotagmin 1 at both excitatory and inhibitory terminals. Single-cell reverse-transcription quantitative PCR analysis revealed that single BCs coexpressed multiple synaptotagmin isoforms, including synaptotagmin 1-5, 7, and 11-13. Our results indicate that, in contrast to excitatory synapses, synaptotagmin 1 is not absolutely required for synchronous release at inhibitory BC-GC synapses. Thus, alternative fast Ca~(2+) sensors contribute to synchronous release of the inhibitory transmitter GABA in cortical circuits.
机译：先前的研究表明，突触标记素1是兴奋性突触中快速同步释放递质的主要Ca〜（2+）传感器。然而，尚未确定在海马抑制突触中Ca〜（2+）传感器的分子身份。为了解决突触结合蛋白1在确定的抑制末端的功能作用，我们从野生型和突触结合蛋白1缺陷型小鼠的器官切片培养物中，通过齿状回中突触连接的篮状细胞（BCs）和颗粒细胞（GC）进行配对记录。正如预期的那样，在兴奋性GC-BC突触中，遗传消除突触素1消除了同步递质释放。但是，保持了抑制性BC-GC突触的同步释放。定量分析表明，消除突触结合蛋白1可以降低释放的可能性和抑制作用，但可以保持BC-GC突触处递质释放的同步性。消除突触结合蛋白1也增加了微型兴奋性突触后电流（以BCs为单位）和微型抑制突触后电流（以GC记录）的频率，这与突触结合蛋白1在兴奋性和抑制性末端的钳制功能一致。单细胞逆转录定量PCR分析显示，单个BC共表达多种突触结合蛋白亚型，包括突触结合蛋白1-5、7和11-13。我们的结果表明，与兴奋性突触相反，在抑制性BC-GC突触中同步释放并非绝对需要突触标记素1。因此，替代性快速Ca〜（2+）传感器有助于抑制皮质电路中抑制性递质GABA的同步释放。

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