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首页> 外文期刊>Neuron >Hippocampal AMPA receptor gating controlled by both TARP and cornichon proteins.
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Hippocampal AMPA receptor gating controlled by both TARP and cornichon proteins.

机译：由TARP和cornichon蛋白控制的海马AMPA受体门控。

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摘要

Transmembrane AMPA receptor regulatory proteins (TARPs) and cornichon proteins (CNIH-2/3) independently modulate AMPA receptor trafficking and gating. However, the potential for interactions of these subunits within an AMPA receptor complex is unknown. Here, we find that TARPs gamma-4, gamma-7, and gamma-8, but not gamma-2, gamma-3, or gamma-5, cause AMPA receptors to "resensitize" upon continued glutamate application. With gamma-8, resensitization occurs with all GluA subunit combinations; however, gamma-8-containing hippocampal neurons do not display resensitization. In recombinant systems, CNIH-2 abrogates gamma-8-mediated resensitization and modifies AMPA receptor pharmacology and gating to match that of hippocampal neurons. In hippocampus, gamma-8 and CNIH-2 associate in postsynaptic densities and CNIH-2 protein levels are markedly diminished in gamma-8 knockout mice. Manipulating neuronal CNIH-2 levels modulates the electrophysiological properties of extrasynaptic and synaptic gamma-8-containing AMPA receptors. Thus, gamma-8 and CNIH-2 functionally interact with common hippocampal AMPA receptor complexes to modulate synergistically kinetics and pharmacology.
机译：跨膜AMPA受体调节蛋白（TARP）和角质蛋白（CNIH-2 / 3）独立调节AMPA受体的转运和门控。但是，AMPA受体复合物中这些亚基相互作用的潜力尚不清楚。在这里，我们发现TARP的gamma-4，gamma-7和gamma-8，而不是gamma-2，gamma-3或gamma-5不会导致AMPA受体在继续应用谷氨酸盐后“重新敏化”。使用gamma-8，所有GluA亚基组合都会发生再敏化;但是，含gamma-8的海马神经元未表现出再敏化作用。在重组系统中，CNIH-2消除了gamma-8介导的再敏化，并修改了AMPA受体药理和门控以匹配海马神经元。在海马中，gamma-8和CNIH-2与突触后密度有关，而在gamma-8基因敲除小鼠中，CNIH-2蛋白水平明显降低。操纵神经元CNIH-2的水平调节突触外和突触gamma-8含AMPA受体的电生理特性。因此，γ-8和CNIH-2在功能上与常见的海马AMPA受体复合物相互作用，以协同调节动力学和药理学。

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