Synapse formation and regulation require interactions between pre- and postsynaptic proteins, notably cell adhesion molecules (CAMs). It has been proposed that the functions of neuroligins (Nlgns), postsynaptic CAMs, rely on the formation of trans-synaptic complexes with neurexins (Nrxns), presynaptic CAMs. Nlgn3 is a unique Nlgn isoform that localizes at both excitatory and inhibitory synapses. However, Nlgn3 function mediated via Nrxn interactions is unknown. Here, we demonstrate that Nlgn3 localizes at postsynaptic sites apposing vesicular glutamate transporter 3-expressing (VGT3+) inhibitory terminals and regulates VGT3+ inhibitory interneuron-mediated synaptic transmission in mouse organotypic slice cultures. Gene expression analysis of interneurons revealed that the αNrxn1+AS4 splice isoform is highly expressed in VGT3+ interneurons as compared with other interneurons. Most importantly, postsynaptic Nlgn3 requires presynaptic αNrxn1+AS4 expressed in VGT3+ interneurons to regulate inhibitory synaptic transmission. Our results indicate that specific Nlgn-Nrxn interactions generate distinct functional properties at synapses.

中文翻译：

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特定的Neuroligin3-αNeurexin1代码调节小鼠海马中的GABA能突触功能。

突触的形成和调节需要突触前和突触后蛋白之间的相互作用，特别是细胞粘附分子（CAMs）。已经提出，神经胶蛋白（Nlgns），突触后CAM的功能依赖于与神经毒素（Nrxns），突触前CAM的反式突触复合物的形成。Nlgn3是独特的Nlgn同种型，既位于兴奋性突触又位于抑制性突触。但是，通过Nrxn相互作用介导的Nlgn3功能是未知的。在这里，我们证明Nlgn3定位在突触后位点的水泡谷氨酸转运蛋白3表达（VGT3 +）抑制终端，并调节VGT3 +抑制间质神经元介导的突触传递在小鼠器官型切片文化。对中间神经元的基因表达分析表明，与其他中间神经元相比，αNrxn1+ AS4剪接异构体在VGT3 +中间神经元中高表达。最重要的是，突触后Nlgn3需要以VGT3 +中间神经元表达的突触前αNrxn1+ AS4来调节抑制性突触传递。我们的结果表明特定的Nlgn-Nrxn相互作用在突触处产生不同的功能特性。