Interrogation and manipulation of Ca2+/CaMK signaling mechanisms underlying cognitive behavior

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H02358
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Neurochemistry/Neuropharmacology
• Research Institution: The University of Tokyo
• Principal Investigator: BITO HARUHIKO 東京大学, 大学院医学系研究科(医学部), 教授 (00291964)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 神経科学 / 脳・神経 / 遺伝子 / シグナル伝達

Outline of Final Research Achievements

In this project, we aimed to obtain mechanistic insights on the Ca2+/calmodulin-dependent information “writing” process that neurons utilize in the living brain. To address this, 1) we developed new improved Ca2+ signaling sensors, and 2) took advantage of these tools to dissect the spread and information processing encoded by Ca2+ signals and Ca2+ effector activation. Furthermore, we investigated the role of Ca2+/calmodulin-dependent signaling in long-term memory consolidation, and identified several new key molecular players involved in this process. These results shed new light on basic principles on how the brain works, and epitomizes the urgent need to developing foundational technologies to record and manipulate brain functions.

Free Research Field

神経生化学