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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Synapse-specific regulation of AMPA receptor function by PSD-95
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Synapse-specific regulation of AMPA receptor function by PSD-95

机译：PSD-95对AMPA受体功能的突触特异性调节

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PSD-95 is a major protein found in virtually all mature excitatory glutamatergic synapses in the brain. Here, we have addressed the role of PSD-95 in controlling glutamatergic synapse function by generating and characterizing a PSD-95 KO mouse. We found that the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) subtype of glutamate receptor (AMPAR)-mediated synaptic transmission was reduced in these mice. Two-photon (2P) uncaging of MNI-glutamate onto individual spines suggested that the decrease in AMPAR function in the PSD-95 KO mouse stems from an increase in the proportion of "silent" synapses i.e., synapses containing N-methyl-D-aspartate (NMDA) receptors (NMDARs) but no AM-PARs. Unexpectedly, the silent synapses in the KO mouse were located onto morphologically mature spines. We also observed that a significant population of synapses appeared unaffected by PSD-95 gene deletion, suggesting that the functional role of PSD-95 displays synapse-specificity. in addition, we report that the decay of NMDAR-mediated current was slower in KO mice: The contribution of NR2B subunit containing receptors to the NMDAR-mediated synaptic current was greater in KO mice. The greater occurrence of silent synapses might be related to the greater magnitude of potentiation after long-term potentiation induction observed in these mice. Together, these results suggest a synapse-specific role for PSD-95 in controlling synaptic function that is independent of spine morphology.
机译：PSD-95是在大脑中几乎所有成熟的兴奋性谷氨酸能突触中发现的主要蛋白质。在这里，我们已经通过生成和表征PSD-95 KO小鼠解决了PSD-95在控制谷氨酸能突触功能中的作用。我们发现，在这些小鼠中，谷氨酸受体（AMPAR）介导的突触传递的α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）亚型减少。 MNI-谷氨酸在单个棘突上的两光子（2P）解构表明，PSD-95 KO小鼠AMPAR功能的降低源于“沉默”突触比例的增加，即突触包含N-甲基-D-天冬氨酸（NMDA）受体（NMDAR），但无AM-PAR。出乎意料的是，KO小鼠中的沉默突触位于形态成熟的棘突上。我们还观察到大量突触似乎不受PSD-95基因缺失的影响，这表明PSD-95的功能作用表现出突触特异性。此外，我们报道了KODAR小鼠中NMDAR介导的电流的衰减较慢：KO小鼠中，含有NR2B亚基的受体对NMDAR介导的突触电流的贡献更大。在这些小鼠中观察到的长期增强诱导后，沉默突触的更大发生可能与增强幅度更大有关。在一起，这些结果表明PSD-95在控制突触功能中的突触特定功能，而该功能与脊柱形态无关。

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