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让记忆持久:突触标记和捕获假说。

Making memories last: the synaptic tagging and capture hypothesis.

机构信息

Laboratory for Cognitive Neuroscience, Centre for Cognitive and Neural Systems, The University of Edinburgh, 1 George Square, Edinburgh EH8 9JZ, UK.

出版信息

Nat Rev Neurosci. 2011 Jan;12(1):17-30. doi: 10.1038/nrn2963.

DOI:10.1038/nrn2963
PMID:21170072
Abstract

The synaptic tagging and capture hypothesis of protein synthesis-dependent long-term potentiation asserts that the induction of synaptic potentiation creates only the potential for a lasting change in synaptic efficacy, but not the commitment to such a change. Other neural activity, before or after induction, can also determine whether persistent change occurs. Recent findings, leading us to revise the original hypothesis, indicate that the induction of a local, synapse-specific 'tagged' state and the expression of long-term potentiation are dissociable. Additional observations suggest that there are major differences in the mechanisms of functional and structural plasticity. These advances call for a revised theory that incorporates the specific molecular and structural processes involved. Addressing the physiological relevance of previous in vitro findings, new behavioural studies have experimentally translated the hypothesis to learning and the consolidation of newly formed memories.

摘要

突触标记和捕获假说认为,蛋白合成依赖性长时程增强的诱导只产生了突触效能持久变化的可能性,但并没有决定是否发生这种变化。在诱导之前或之后的其他神经活动也可以决定是否发生持久的变化。最近的发现促使我们修改了最初的假说,表明诱导局部、突触特异性的“标记”状态和长时程增强的表达是可分离的。其他观察结果表明,功能和结构可塑性的机制有很大的不同。这些进展要求提出一个新的理论,将涉及的特定分子和结构过程纳入其中。为了解决以前体外发现的生理相关性问题,新的行为研究已经将该假说应用于学习和新形成记忆的巩固。

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本文引用的文献

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Relevance of synaptic tagging and capture to the persistence of long-term potentiation and everyday spatial memory.突触标记和捕获与长时程增强和日常空间记忆的持久性的相关性。
Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19537-42. doi: 10.1073/pnas.1008638107. Epub 2010 Oct 20.
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Protein degradation by the proteasome is required for synaptic tagging and the heterosynaptic stabilization of hippocampal late-phase long-term potentiation.蛋白酶体介导的蛋白质降解对于突触标记和海马体晚期长时程增强的异突触稳定是必需的。
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Long-term potentiation-induced changes in actin dynamics and spine geometry persist on the timescale of the synaptic tag.长时程增强诱导的肌动蛋白动力学和棘突几何形状的变化在突触标记的时间尺度上持续存在。
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Genetic inactivation of the Translin/Trax RNase activity alters small RNAs including miRNAs, disrupts gene expression and impairs distinct forms of hippocampal synaptic plasticity and memory.转运蛋白/转录激活蛋白(Translin/Trax)核糖核酸酶活性的基因失活会改变包括微小RNA(miRNA)在内的小RNA,破坏基因表达,并损害海马体突触可塑性和记忆的不同形式。
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Heterosynaptic interactions between dorsal and ventral hippocampus in individual medium spiny neurons of the nucleus accumbens ventromedial shell.伏隔核腹内侧壳层单个中等棘状神经元中背侧和腹侧海马体之间的异突触相互作用。
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Thalamic input to the lateral amygdala determines the temporal window of fear-memory association.丘脑向杏仁核外侧的输入决定了恐惧记忆关联的时间窗口。
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Synaptic tagging and capture: differential role of distinct calcium/calmodulin kinases in protein synthesis-dependent long-term potentiation.突触标记和捕获:不同的钙/钙调蛋白激酶在蛋白合成依赖性长时程增强中的作用差异。
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Spatially restricting gene expression by local translation at synapses.通过突触处的局部翻译来限制空间基因表达。
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Autophosphorylated CaMKIIalpha acts as a scaffold to recruit proteasomes to dendritic spines.自磷酸化的 CaMKIIalpha 作为支架将蛋白酶体募集到树突棘。
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Interfering with the actin network and its effect on long-term potentiation and synaptic tagging in hippocampal CA1 neurons in slices in vitro.干扰肌动蛋白网络及其对体外脑片中海马CA1神经元长时程增强和突触标记的影响。
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Behavioral tagging is a general mechanism of long-term memory formation.行为标记是长期记忆形成的一种普遍机制。
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