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2014-05-15 神经生物学前沿学术报告系列 Yasunori Hayashi

 

报告题目:Roles of cytoskeleton in hippocampal synaptic plasticity

 

报告人: Yasunori Hayashi  Ph.D.

Team Leader,Brain Science Institute,RIKEN,Japan.

时间:   2014年5月19日(周一),下午14:00-15:30

地点:   西区生物楼329会议室

主办单位:中国科学技术大学生命科学学院

合肥微尺度物质科学国家实验室

中国科学院脑功能与脑疾病重点实验室

 

报告简介: Synaptic plasticity occurs as a result of biochemical reactions and protein interactions that take place within small volume of less than 1fl. Application of traditional biochemical approaches is simply impractical to elucidate the process of synaptic plasticity. We therefore employed optical methods including FRET, FLIM, photoactivatable proteins and caged compounds to elucidate the mechanism of synaptic plasticity, with an emphasis on structural modification of dendritic spine seen during long-term potentiation (LTP) of hippocampal CA1 pyramidal neurons. After the induction of LTP, the remodeling of actin cytoskeleton and its polymerization is the first thing to happen. Active cofilin is massively transported to the spine and severs the F-actin, which likely generates new free ends of actin from where new filament starts growing. Thereafter, these two proteins forms a stable complex at the base of spine head thereby forming a stable F-actin and regulating spine expansion. In contrast, the postsynaptic density (PSD) was independently remodeled, as PSD scaffolding proteins did not change their amount and localization until late protein synthesis-dependent third phase. Our findings show how and when spine substructures are remodeled during LTP and explain why synaptic plasticity rules change over time.


 

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