Dynamics of glutamate receptor during synaptic plasticity

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04259
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Kyoto University
• Principal Investigator: Hirano Tomoo 京都大学, 理学研究科, 教授 (50181178)
• Co-Investigator(Renkei-kenkyūsha): TANAKA Hiromitsu 京都大学, 大学院理学研究科, 助教 (30705447)
• Research Collaborator: FUJII Shumpei ; FUNAHASHI Junichiro ; SAKAGUCHI Daiki ; MORI Tomomi
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: シナプス可塑性 / グルタミン酸受容体 / エキソサイトーシス / エンドサイトーシス / 海馬 / 蛍光イメージング / 長期増強 / 長期抑圧

Outline of Final Research Achievements

We have studied expression mechanism of long-term depression (LTD) using a novel experimental method we developed. LTD is a type of synaptic plasticity, which is a cellular basis of learning and memory. The LTD expression is accompanied by the decrease in number of postsynaptic AMPA-type glutamate receptor, which was suggested to be caused by enhancement of endocytosis. We labelled AMPA receptor (AMPAR) with fluorescent protein SEP, and performed live-cell imaging of AMPAR-SEP in cultured hippocampal neurons. The new method enabled us to visualize individual endo- and exocytosis of AMPAR with a high signal to noise ratio and high spatiotemporal resolution. The results indicate that hippocampal LTD is primarily caused not by the enhancement of AMPAR endocytosis but by the suppression of AMPAR exocytosis.

Free Research Field

神経科学