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首页> 外文期刊>Neuron >Synapse-specific and developmentally regulated targeting of AMPA receptors by a family of MAGUK scaffolding proteins.
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Synapse-specific and developmentally regulated targeting of AMPA receptors by a family of MAGUK scaffolding proteins.

机译：MAGUK脚手架蛋白家族对AMPA受体的突触特异性和发育调控。

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摘要

Trafficking of AMPA receptors (AMPA-Rs) to and from synapses controls the strength of excitatory synaptic transmission. However, proteins that cluster AMPA-Rs at synapses remain poorly understood. Here we show that PSD-95-like membrane-associated guanylate kinases (PSD-MAGUKs) mediate this synaptic targeting, and we uncover a remarkable functional redundancy within this protein family. By manipulating endogenous neuronal PSD-MAGUK levels, we find that both PSD-95 and PSD-93 independently mediate AMPA-R targeting at mature synapses. We also reveal unanticipated synapse heterogeneity as loss of either PSD-95 or PSD-93 silences largely nonoverlapping populations of excitatory synapses. In adult PSD-95 and PSD-93 double knockout animals, SAP-102 is upregulated and compensates for the loss of synaptic AMPA-Rs. At immature synapses, PSD-95 and PSD-93 play little role in synaptic AMPA-R clustering; instead, SAP-102 dominates. These studies establish a PSD-MAGUK-specific regulation of AMPA-R synaptic expression that establishes and maintains glutamatergic synaptic transmission in the mammalian central nervous system.
机译：AMPA受体（AMPA-Rs）往返突触的运输控制了兴奋性突触传递的强度。然而，在突触处聚集AMPA-R的蛋白质仍知之甚少。在这里，我们显示了PSD-95样膜相关鸟苷酸激酶（PSD-MAGUKs）介导了这种突触靶向，并且我们发现了该蛋白家族中的显着功能冗余。通过操纵内源性神经元PSD-MAGUK的水平，我们发现PSD-95和PSD-93都可以独立介导针对成熟突触的AMPA-R。我们还揭示了意料之外的突触异质性，因为PSD-95或PSD-93的丢失使大部分非重叠的兴奋性突触沉默。在成年PSD-95和PSD-93双基因敲除动物中，SAP-102被上调并补偿突触AMPA-R的损失。在未成熟的突触中，PSD-95和PSD-93在突触AMPA-R聚类中起很小的作用。相反，SAP-102占主导地位。这些研究建立了AMPA-R突触表达的PSD-MAGUK特异性调控，该调控在哺乳动物中枢神经系统中建立和维持谷氨酸能突触传递。

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