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通过激活含 GluA3 的 AMPA 受体实现突触可塑性。

Synaptic plasticity through activation of GluA3-containing AMPA-receptors.

机构信息

Synaptic Plasticity and Behavior Group, The Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands.

出版信息

Elife. 2017 Aug 1;6:e25462. doi: 10.7554/eLife.25462.

DOI:10.7554/eLife.25462
PMID:28762944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5578739/
Abstract

Excitatory synaptic transmission is mediated by AMPA-type glutamate receptors (AMPARs). In CA1 pyramidal neurons of the hippocampus two types of AMPARs predominate: those that contain subunits GluA1 and GluA2 (GluA1/2), and those that contain GluA2 and GluA3 (GluA2/3). Whereas subunits GluA1 and GluA2 have been extensively studied, the contribution of GluA3 to synapse physiology has remained unclear. Here we show in mice that GluA2/3s are in a low-conductance state under basal conditions, and although present at synapses they contribute little to synaptic currents. When intracellular cyclic AMP (cAMP) levels rise, GluA2/3 channels shift to a high-conductance state, leading to synaptic potentiation. This cAMP-driven synaptic potentiation requires the activation of both protein kinase A (PKA) and the GTPase Ras, and is induced upon the activation of β-adrenergic receptors. Together, these experiments reveal a novel type of plasticity at CA1 hippocampal synapses that is expressed by the activation of GluA3-containing AMPARs.

摘要

兴奋性突触传递由 AMPA 型谷氨酸受体 (AMPARs) 介导。在海马 CA1 锥体神经元中，两种类型的 AMPAR 占主导地位：一种含有 GluA1 和 GluA2 亚基（GluA1/2），另一种含有 GluA2 和 GluA3 亚基（GluA2/3）。虽然亚基 GluA1 和 GluA2 已经得到了广泛研究，但 GluA3 对突触生理学的贡献仍不清楚。在这里，我们在小鼠中表明，GluA2/3 在基础条件下处于低电导状态，尽管存在于突触中，但对突触电流的贡献很小。当细胞内环磷酸腺苷 (cAMP) 水平升高时，GluA2/3 通道转变为高电导状态，导致突触增强。这种 cAMP 驱动的突触增强需要蛋白激酶 A (PKA) 和 GTPase Ras 的激活，并在 β-肾上腺素能受体激活时诱导。这些实验共同揭示了 CA1 海马突触的一种新型可塑性，这种可塑性是通过激活含有 GluA3 的 AMPAR 表达的。

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