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首页> 外文期刊>Neuron >C. elegans Punctin Clusters GABA(A) Receptors via Neuroligin Binding and UNC-40/DCC Recruitment
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C. elegans Punctin Clusters GABA(A) Receptors via Neuroligin Binding and UNC-40/DCC Recruitment

机译：秀丽隐杆线虫突触簇GABA（A）受体通过神经胶蛋白结合和UNC-40 / DCC招聘。

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摘要

Positioning type A GABA receptors (GABA(A)Rs) in front of GABA release sites sets the strength of inhibitory synapses. The evolutionarily conserved Ce-Punctin/MADD-4 is an anterograde synaptic organizer that specifies GABAergic versus cholinergic identity of postsynaptic domains at the C. elegans neuromuscular junctions (NMJs). Here we show that the Ce-Punctin secreted by GABAergic motor neurons controls the clustering of GABAARs through the synaptic adhesion molecule neuroligin (NLG-1) and the netrin receptor UNC-40/DCC. The short isoform of Ce-Punctin binds and clusters NLG-1 postsynaptically at GABAergic NMJs. NLG-1 disruption causes a strong reduction of GABA(A)R content at GABAergic synapses. Ce-Punctin also binds and localizes UNC-40 receptors in the postsynaptic membrane of NMJs, which promotes the recruitment of GABA(A)Rs by NLG-1. Since the mammalian orthologs of these genes are expressed in the central nervous system and their mutations are implicated in neuropsychiatric diseases, this molecular pathway might have been evolutionarily conserved.
机译：在GABA释放位点前面放置A型GABA受体（GABA（A）Rs）可设置抑制突触的强度。进化上保守的Ce-Punctin / MADD-4是顺行的突触组织者，在秀丽隐杆线虫神经肌肉接头（NMJs）上指定突触后结构域的GABA能与胆碱能同一性。在这里，我们显示由GABA能动神经元分泌的Ce-Punctin通过突触粘附分子Neuroligin（NLG-1）和netrin受体UNC-40 / DCC控制GABAAR的聚类。 Ce-突触素的短同工型在GABA能NMJs后突触结合并聚集NLG-1。 NLG-1破坏会导致GABA能突触中GABA（A）R含量大大降低。 Ce-Punctin还结合并定位NMJs突触后膜中的UNC-40受体，这会促进NLG-1募集GABA（A）Rs。由于这些基因的哺乳动物直系同源基因在中枢神经系统中表达，并且它们的突变与神经精神疾病有关，因此该分子途径可能在进化上是保守的。

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