2017 Fiscal Year Annual Research Report

NMDA受容体依存性LTPの制御のための光プローブの作成

Publicly Offered Research

Project Area	Resonance Biology for Innovative Bioimaging
Project/Area Number	16H01438
Research Institution	Kyoto University
Principal Investigator	林康紀京都大学, 医学研究科, 教授 (90466037)
Project Period (FY)	2016-04-01 – 2018-03-31
Keywords	細胞骨格 / シナプス可塑性 / 記憶固定化 / 長期記憶 / 光増感法 / コフィリン
Outline of Annual Research Achievements	Memory is retained in the hippocampus after initial learning. It is then transferred to the cortex where it is permanently stored. Although it has been speculated that LTP-like mechanism is involved in this process, there has been no information when and where it happens. We previously found that in the initial phase of LTP, cofilin is transported to the spine and persistently accumulates. Therefore, we assume that cofilin-dependent synaptic plasticity plays an important role in memory consolidation. In order to inactivate cofilin, we employed a genetically encoded photosensitizer, SuperNova. To validate this system, structural LTP was induced with two-photon (2P) uncaging of MNI-glutamate in the single dendritic spine, which expresses SN-fused cofilin (CFL-SN). Followed illumination at 10 min after LTP induction, the spine volume decreased. The decrease in the spine volume was also observed up to 30 min but not at 50 min. Furthermore, the laser irradiation on the spine 1 min before sLTP had no effect on the spine enlargement. These results indicate cofilin is critical for maintenance of LTP up to 30 min after induction, and the inactivation of cofilin had negligible effect on LTP induction and the volume of unstimulated spine. We confirmed electrically recorded LTP is canceled by recording field EPSP from stratum radiatum of CA1.
Research Progress Status	29年度が最終年度であるため、記入しない。
Strategy for Future Research Activity	29年度が最終年度であるため、記入しない。