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本文引用的文献

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Phosphorylation of cAMP response element-binding protein in hippocampal neurons as a protective response after exposure to glutamate in vitro and ischemia in vivo.海马神经元中环磷酸腺苷反应元件结合蛋白的磷酸化作为体外暴露于谷氨酸和体内缺血后的一种保护反应。
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Is LTP in the hippocampus a useful model for learning-related alterations in gene expression?海马体中的长时程增强(LTP)是学习相关基因表达变化的有用模型吗?
Rev Neurosci. 2001;12(3):289-96. doi: 10.1515/revneuro.2001.12.3.289.
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Activation of silent synapses by rapid activity-dependent synaptic recruitment of AMPA receptors.通过快速的活动依赖性AMPA受体突触募集激活沉默突触。
J Neurosci. 2001 Aug 15;21(16):6008-17. doi: 10.1523/JNEUROSCI.21-16-06008.2001.
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Interaction with the NMDA receptor locks CaMKII in an active conformation.与NMDA受体的相互作用会使CaMKII处于激活构象。
Nature. 2001 Jun 14;411(6839):801-5. doi: 10.1038/35081080.
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Long-lasting hippocampal potentiation and contextual memory consolidation.持久的海马体突触增强与情境记忆巩固。
Eur J Neurosci. 2001 Jun;13(12):2291-8. doi: 10.1046/j.0953-816x.2001.01609.x.
6
Alpha-CaMKII-dependent plasticity in the cortex is required for permanent memory.永久性记忆需要皮质中α-钙调蛋白依赖性蛋白激酶II(α-CaMKII)介导的可塑性。
Nature. 2001 May 17;411(6835):309-13. doi: 10.1038/35077089.
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Densin-180 forms a ternary complex with the (alpha)-subunit of Ca2+/calmodulin-dependent protein kinase II and (alpha)-actinin.致密素-180与Ca2+/钙调蛋白依赖性蛋白激酶II的α亚基和α辅肌动蛋白形成三元复合物。
J Neurosci. 2001 Jan 15;21(2):423-33. doi: 10.1523/JNEUROSCI.21-02-00423.2001.
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Retrograde amnesia for spatial memory induced by NMDA receptor-mediated long-term potentiation.NMDA受体介导的长时程增强诱导的空间记忆逆行性遗忘。
J Neurosci. 2001 Jan 1;21(1):356-62. doi: 10.1523/JNEUROSCI.21-01-00356.2001.
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Involvement of the secretory pathway for AMPA receptors in NMDA-induced potentiation in hippocampus.海马体中N-甲基-D-天冬氨酸(NMDA)诱导的增强作用中,AMPA受体分泌途径的参与情况。
J Neurosci. 2001 Jan 1;21(1):27-34. doi: 10.1523/JNEUROSCI.21-01-00027.2001.
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Protein kinase C activation modulates alpha-calmodulin kinase II binding to NR2A subunit of N-methyl-D-aspartate receptor complex.蛋白激酶C激活调节α-钙调蛋白激酶II与N-甲基-D-天冬氨酸受体复合物NR2A亚基的结合。
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钙/钙调蛋白依赖性蛋白激酶II在神经元可塑性和记忆形成中的作用。

Participation of CaMKII in neuronal plasticity and memory formation.

作者信息

Cammarota Martín, Bevilaqua Lia R M, Viola Haydée, Kerr Daniel S, Reichmann Bruno, Teixeira Viviane, Bulla Mário, Izquierdo Iván, Medina Jorge H

机构信息

Centro de Memória, Departamento de Bioquímica, ICBS, UFRGS, Porto Alegre, Brasil.

出版信息

Cell Mol Neurobiol. 2002 Jun;22(3):259-67. doi: 10.1023/a:1020763716886.

DOI:10.1023/a:1020763716886
PMID:12469869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11533765/
Abstract
  1. The unique biochemical properties of Ca(2+)/calmodulin (CaM)-dependent protein kinase II have made this enzyme one of the paradigmatic models of the forever searched "memory molecule." 2. In particular, the central participation of CaMKII as a sensor of the Ca(2+) signals generated by activation of NMDA receptors after the induction of long-term plastic changes, has encouraged the use of pharmacological, genetic, biochemical, and imaging tools to unveil the role of this kinase in the acquisition, consolidation, and expression of different types of memories. 3. Here we review some of the more exciting discoveries related to the mechanisms involved in CaMKII activation and synaptic plasticity.
摘要
  1. Ca(2+)/钙调蛋白(CaM)依赖性蛋白激酶II独特的生化特性,使其成为一直以来所探寻的“记忆分子”的典型模型之一。2. 特别是,在长期可塑性变化诱导后,CaMKII作为N-甲基-D-天冬氨酸(NMDA)受体激活所产生的Ca(2+)信号的传感器发挥核心作用,这促使人们运用药理学、遗传学、生物化学和成像工具来揭示该激酶在不同类型记忆的获取、巩固和表达中的作用。3. 在此,我们回顾一些与CaMKII激活及突触可塑性相关机制的更令人兴奋的发现。