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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Synapse formation and clustering of neuroligin-2 in the absence of GABA_A receptors
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Synapse formation and clustering of neuroligin-2 in the absence of GABA_A receptors

机译：在没有GABA_A受体的情况下神经胶蛋白2的突触形成和聚集

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摘要

GABAergic synapses are crucial for brain function, but the mechanisms underlying inhibitory synaptogenesis are unclear. Here, we show that postnatal Purkinje cells (PCs) of GABA_A α 1 knockout (KO) mice express transiently the α3 subunit, leading to the assembly of functional GABA_A receptors and initial normal formation of inhibitory synapses, that are retained until adulthood. Subsequently, down-regulation of the α3 subunit causes a complete loss of GABAergic postsynaptic currents, resulting in a decreased rate of inhibitory synaptogenesis and formation of mismatched synapses between GABAergic axons and PC spines. Notably, the postsynaptic adhesion molecule neuroligin-2 (NL2) is correctly targeted to inhibitory synapses lacking GABA_A receptors and the scaffold molecule gephyrin, but is absent from mismatched synapses, despite innervation by GABAergic axons. Our data indicate that GABAa receptors are dispensable for synapse formation and maintenance and for targeting NL2 to inhibitory synapses. However, GABAergic signaling appears to be crucial for activity-dependent regulation of synapse density during neuronal maturation.
机译：GABA能突触对脑功能至关重要，但抑制性突触发生的机制尚不清楚。在这里，我们显示了GABA_Aα1敲除（KO）小鼠的产后Purkinje细胞（PC）瞬时表达α3亚基，导致功能性GABA_A受体的组装和抑制突触的初始正常形成，直至成年。随后，α3亚基的下调导致GABA能突触后电流的完全丧失，从而导致抑制性突触发生率降低以及GABA能轴突和PC棘之间失配突触的形成。值得注意的是，突触后粘附分子Neuroligin-2（NL2）正确地靶向缺乏GABA_A受体和支架分子gephyrin的抑制性突触，但是尽管GABA能轴突支配了神经，但突触失配却不存在。我们的数据表明，GABA a受体对于突触的形成和维持以及将NL2靶向抑制性突触而言都是可有可无的。但是，GABA能信号似乎对神经元成熟过程中依赖活性的突触密度调节至关重要。

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