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首页> 外文期刊>Neuropharmacology >Forgetting of what was once learned: Exploring the role of postsynaptic ionotropic glutamate receptors on memory formation, maintenance, and decay
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Forgetting of what was once learned: Exploring the role of postsynaptic ionotropic glutamate receptors on memory formation, maintenance, and decay

机译:忘记了曾经学习的内容:探索突触后离子级谷氨酸受体对记忆形成,维护和腐烂的作用

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Over the past years, extensive research in experimental cognitive neuroscience has provided a comprehensive understanding about the role of ionotropic glutamate receptor (IGluR)-dependent signaling underpinning postsynaptic plasticity induced by long-term potentiation (LTP), the leading cellular basis of long-term memory (LTM). However, despite the fact that iGluR-mediated postsynaptic plasticity regulates the formation and persistence of LTP and LTM, here we discuss the state-of-the-art regarding the mechanisms underpinning both LTP and LTM decay. First, we review the crucial roles that iGluRs play on memory encoding and stabilization. Second, we discuss the latest findings in forgetting considering hippocampal GluA2-AMPAR trafficking at postsynaptic sites as well as dendritic spine remodeling possibly involved in LTP decay. Third, on the role of retrieving consolidated LTMs, we discuss the mechanisms involved in memory destabilization that occurs followed reactivation that share striking similarities with the neurobiological basis of forgetting. Fourth, since different AMPAR subunits as well as postsynaptic scaffolding proteins undergo ubiquitination, the ubiquitin-proteasome system (UPS) is discussed in light of memory decay. In conclusion, we provide an integrated overview revealing some of the mechanisms determining memory forgetting that are mediated by iGluRs. This article is part of the Special Issue entitled 'Ionotropic glutamate receptors'. (C) 2016 Elsevier Ltd. All rights reserved.
机译:在过去几年中,在实验认知神经科学的广泛研究已经综合了解关于离子级谷氨酸受体(IGLUR) - 依赖性信号传导的基础突触型胸膜塑性,长期促销(LTP),即长期的主要蜂窝基础内存(LTM)。然而,尽管IGLUR介导的后腹膜塑性调节LTP和LTM的形成和持续性,但在这里,我们讨论了基于LTP和LTM衰变的机制的最新技术。首先,我们审查iglurs在内存编码和稳定上发挥的重要角色。其次,我们讨论了忘记考虑突触后突触网站的海马Glua2-AMPAR以及可能参与LTP衰减的树突脊柱重塑的最新发现。第三,就检索综合LTMS的作用,我们讨论了记忆稳定化的机制,这种机制发生遵循重新激活,这些重新激活与忘记的神经生物学的基础共享醒目的相似之处。第四,由于不同的AMPAR亚基以及突触后支架蛋白质经历泛素化,因此鉴于记忆衰减而讨论了遍突蛋白 - 蛋白酶体系(UPS)。总之,我们提供了一个综合概述,揭示了一些确定内存遗忘的机制,该机制由iGlurs介导。本文是标题为“离子型谷氨酸受体”的特刊的一部分。 (c)2016 Elsevier Ltd.保留所有权利。

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