Cornichon2 Dictates the Time Course of Excitatory Transmission at Individual Hippocampal Synapses
Cornichon2 Dictates the Time Course of Excitatory Transmission at Individual Hippocampal Synapses
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DOI：
10.1016/j.neuron.2014.03.031
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发表时间：
2014-05-21
期刊：
影响因子：
16.2
通讯作者：
Fakler, Bernd
中科院分区：
文献类型：
--
作者：
Boudkkazi, Sami;Brechet, Aline;Fakler, Bernd
Cornichon2 （CNIH2）是哺乳动物大脑中AMPA受体（AMPAR）复合物的一个组成部分，可以减缓异源重组受体通道的失活和脱敏。然而，它在神经元信号转导中的意义仍然难以捉摸。本研究通过配对记录显示，含cnih2的ampar决定了苔藓纤维扣（MFB）单动作电位在海马体门状苔藓细胞中引发的兴奋性突触后电流（EPSCs）的缓慢衰减。选择性敲除CNIH2可显著加速单个mfb苔藓细胞突触的EPSC，但不会改变EPSC的振幅。相比之下，缺乏CNIH2表达的MFBs和突起中间神经元之间突触中快速衰减的EPSCs不受蛋白敲除的影响，但被病毒定向表达的CNIH2减缓。这些结果确定了CNIH2是慢速和快速EPSC表型之间的分子区别，并表明CNIH2影响时间过程，从而影响兴奋性突触传递的有效性。
Cornichon2 (CNIH2), an integral component of AMPA receptor (AMPAR) complexes in the mammalian brain, slows deactivation and desensitization of heterologously reconstituted receptor channels. Its significance in neuronal signal transduction, however, has remained elusive. Here we show by paired recordings that CNIH2-containing AMPARs dictate the slow decay of excitatory postsynaptic currents (EPSCs) elicited in hilar mossy cells of the hippocampus by single action potentials in mossy fiber boutons (MFB). Selective knockdown of CNIH2 markedly accelerated EPSCs in individual MFB-mossy cell synapses without altering the EPSC amplitude. In contrast, the rapidly decaying EPSCs in synapses between MFBs and aspiny interneurons that lack expression of CNIH2 were unaffected by the protein knockdown but were slowed by virus-directed expression of CNIH2. These results identify CNIH2 as the molecular distinction between slow and fast EPSC phenotypes and show that CNIH2 influences the time course and, hence, the efficacy of excitatory synaptic transmission.