増大特集 記憶と忘却に関わる脳のしくみ-分子機構から健忘の症候まで 学習・記憶の細胞基盤-シナプス・アンサンブルを可視化・操作する技術の創出
増大特集 記憶と忘却に関わる脳のしくみ-分子機構から健忘の症候まで 学習・記憶の細胞基盤-シナプス・アンサンブルを可視化・操作する技術の創出
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特色:参与记忆和遗忘的大脑机制 - 从分子机制到健忘症的症状学习和记忆的细胞基础 - 创建可视化和操纵突触整体的技术
DOI:
10.11477/mf.1416201072
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发表时间:
2018
期刊:
影响因子:
--
通讯作者:
林(高木) 朗子
中科院分区:
文献类型:
--
作者:
佐藤 壮泰;宮本 成美;千葉 久実;小尾 紀翔;林(高木) 朗子
Dentritic spines are small membrane protrusions. Their regulation is thought to be important for memory storage, but the links between dentric spines and memory have been largely correlational because of a luck of techniques for manipulating individual spines. To overcome this problem, we have developed a novel synaptic optoprobe, AS-PaRac1, which is unique not only because it specifically labels recently potentiated spines, but also because it becomes possible to selectively shrink spines containing AS-PaRac1. This indicates that AS-PaRac1 can be use to specifically visualize the recently" written spines" and that the erasure of these spines is possible upon excitation with blue light. Using in vivo two-photon imaging, synaptic potentiation was visualized during active remodeling of the neocortex. Upon learning a motor skill, AS-PaRac1 expression was induced in a relatively small number of neurons, in which approximately 8% of spines were tagged by AS-PaRac1. The labeled spines were broadly distributed throughout the dendritic tree. Excitation with blue light induced shrinkage of learning related spines and disrupted the acquired motor learning. In contrast, the erasure of a similar number of learning-irrelevant spines did not affect task performance. This novel light-dependent tool will open up new areas of memory research, and will additionally shed light on the neural networks that determine who we are.