Analysis of neuro-glial interactions via extracellular ion signals

2023 Fiscal Year Final Research Report

• Project/Area Number: 17K17615
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Basic / Social brain science; General physiology
• Research Institution: Yamagata University
• Principal Investigator: Goto Jun-Ichi 山形大学, 医学部, 助教 (70435650)
• Project Period (FY): 2017-04-01 – 2024-03-31
• Keywords: シナプス可塑性 / イノシトール三リン酸 / カルシウムシグナル

Outline of Final Research Achievements

Although preliminary data were obtained from simultaneous measurements of extracellular ion concentrations and synaptic plasticity, it was difficult to record the data with high precision. Thus we changed the original plan and published the related research results.
We examined depotentiation and LTP inhibition of hippocampal synapses in IRBIT KO mice, which are downstream of IP3 receptor signaling, and found that both depotentiation and LTP inhibition were inhibited in IRBIT KO mice, that was the same as in IP3 receptor KO mice. On the other hand, short tetanus LTP, which was enhanced in IP3 receptor KO mice, was not changed in IRBIT KO mice, suggesting that another pathway downstream of the IP3 receptor is involved.

Free Research Field

神経生理学

Academic Significance and Societal Importance of the Research Achievements

本研究成果は記憶・学習における神経系の基盤であるシナプス可塑性とカルシウムシグナル及びIP3シグナルがどのように関連するかの一端を明らかにしたものである。カルシウムシグナルが記憶・学習に果たす役割については広範で詳細な研究がなされているが、それに比べるとIP3シグナルの果たす役割についての理解は限定的である。本研究では特にIP3シグナルが従来型のカルシウムシグナルに非依存的にシナプス可塑性を制御していることを明らかにしており、記憶・学習の細胞基盤の多様性について新たな知見を提供するものである。