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首页> 外文期刊>Neuron >Neuroligin 2 drives postsynaptic assembly at perisomatic inhibitory synapses through gephyrin and collybistin.
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Neuroligin 2 drives postsynaptic assembly at perisomatic inhibitory synapses through gephyrin and collybistin.

机译：Neuroligin 2通过gephyrin和collybistin在过抑制抑制的突触中驱动突触后组装。

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摘要

In the mammalian CNS, each neuron typically receives thousands of synaptic inputs from diverse classes of neurons. Synaptic transmission to the postsynaptic neuron relies on localized and transmitter-specific differentiation of the plasma membrane with postsynaptic receptor, scaffolding, and adhesion proteins accumulating in precise apposition to presynaptic sites of transmitter release. We identified protein interactions of the synaptic adhesion molecule neuroligin 2 that drive postsynaptic differentiation at inhibitory synapses. Neuroligin 2 binds the scaffolding protein gephyrin through a conserved cytoplasmic motif and functions as a specific activator of collybistin, thus guiding membrane tethering of the inhibitory postsynaptic scaffold. Complexes of neuroligin 2, gephyrin and collybistin are sufficient for cell-autonomous clustering of inhibitory neurotransmitter receptors. Deletion of neuroligin 2 in mice perturbs GABAergic and glycinergic synaptic transmission and leads to a loss of postsynaptic specializations specifically at perisomatic inhibitory synapses.
机译：在哺乳动物的CNS中，每个神经元通常会从不同种类的神经元中接收数千个突触输入。突触向突触后神经元的传递依赖于质膜的局部和递质特异性分化，其中突触后受体，支架和粘附蛋白以精确的方式积累在递质释放的突触前部位。我们确定了突触粘附分子neuroligin 2的蛋白相互作用，该蛋白在抑制性突触中驱动突触后分化。 Neuroligin 2通过保守的胞质基序与脚手架蛋白gephyrin结合，并起胶体蛋白的特异性激活剂的作用，从而指导抑制性突触后支架的膜束缚。 Neuroligin 2，gephyrin和collybistin的复合物足以抑制抑制性神经递质受体的细胞自主聚集。小鼠神经胶蛋白2的缺失会扰乱GABA能和甘氨酸能的突触传递，并导致突触后专一性丧失，特别是在perisomatic抑制性突触处。

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