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III 型代谢型谷氨酸受体控制大鼠海马 CA2 区的长时程增强和突触标记/捕获。

Group III metabotropic glutamate receptors gate long-term potentiation and synaptic tagging/capture in rat hippocampal area CA2.

机构信息

Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.

Life Sciences Institute Neurobiology Programme, National University of Singapore, Singapore, Singapore.

出版信息

Elife. 2020 Apr 20;9:e55344. doi: 10.7554/eLife.55344.

DOI:10.7554/eLife.55344
PMID:32310084
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7170650/
Abstract

Metabotropic glutamate receptors (mGluRs) play an important role in synaptic plasticity and memory and are largely classified based on amino acid sequence homology and pharmacological properties. Among group III metabotropic glutamate receptors, mGluR7 and mGluR4 show high relative expression in the rat hippocampal area CA2. Group III metabotropic glutamate receptors are known to down-regulate cAMP-dependent signaling pathways via the activation of G proteins. Here, we provide evidence that inhibition of group III mGluRs by specific antagonists permits an NMDA receptor- and protein synthesis-dependent long-lasting synaptic potentiation in the apparently long-term potentiation (LTP)-resistant Schaffer collateral (SC)-CA2 synapses. Moreover, long-lasting potentiation of these synapses transforms a transient synaptic potentiation of the entorhinal cortical (EC)-CA2 synapses into a stable long-lasting LTP, in accordance with the synaptic tagging/capture hypothesis (STC). Furthermore, this study also sheds light on the role of ERK/MAPK protein signaling and the downregulation of STEP protein in the group III mGluR inhibition-mediated plasticity in the hippocampal CA2 region, identifying them as critical molecular players. Thus, the regulation of group III mGluRs provides a conducive environment for the SC-CA2 synapses to respond to events that could lead to activity-dependent synaptic plasticity.

摘要

代谢型谷氨酸受体（mGluRs）在突触可塑性和记忆中发挥重要作用，主要根据氨基酸序列同源性和药理学特性进行分类。在 III 组代谢型谷氨酸受体中，mGluR7 和 mGluR4 在大鼠海马 CA2 区表现出相对较高的表达。已知 III 组代谢型谷氨酸受体通过激活 G 蛋白下调 cAMP 依赖性信号通路。在这里，我们提供的证据表明，通过特定的拮抗剂抑制 III 组 mGluRs 可允许 NMDA 受体和蛋白质合成依赖性的持久突触增强作用在明显的长时程增强（LTP）抗性 Schaffer 侧支（SC）-CA2 突触中发生。此外，这些突触的长时程增强将暂时的内嗅皮质（EC）-CA2 突触的突触增强转化为稳定的持久 LTP，符合突触标记/捕获假说（STC）。此外，这项研究还阐明了 ERK/MAPK 蛋白信号和 STEP 蛋白下调在海马 CA2 区 III 组 mGluR 抑制介导的可塑性中的作用，将它们鉴定为关键的分子参与者。因此，III 组 mGluRs 的调节为 SC-CA2 突触提供了有利的环境，以响应可能导致活性依赖性突触可塑性的事件。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/010d1eac4650/elife-55344-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/47d7a4641a9d/elife-55344-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/f63ab725cb08/elife-55344-fig2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/3e9e12db9e59/elife-55344-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/1861233a365a/elife-55344-fig3-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/9a99fec54975/elife-55344-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/73309fe61e47/elife-55344-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/4be271fcf8a6/elife-55344-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/010d1eac4650/elife-55344-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/47d7a4641a9d/elife-55344-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/f63ab725cb08/elife-55344-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/65ee92328391/elife-55344-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/3c7c024fba51/elife-55344-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/3e9e12db9e59/elife-55344-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/1861233a365a/elife-55344-fig3-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/9a99fec54975/elife-55344-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/73309fe61e47/elife-55344-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf4/7170650/4be271fcf8a6/elife-55344-fig6.jpg
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