The role of AMPA receptor GluR1 for rapid-acting antidepressant behavior

Research Project

Project/Area Number	26860481
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	General internal medicine(including psychosomatic medicine)
Research Institution	Yamaguchi University
Principal Investigator	HOBARA Teruyuki 山口大学, 医学部, 特別医学研究員 (20637970)
Project Period (FY)	2014-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000) Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000) Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords	CaMKIIβ / ストレス / うつ病 / 抗うつ作用 / GluR1 / 抗うつ効果 / depression
Outline of Final Research Achievements	aThe aim of this study is to elucidate the molecular mechanism underlying HDAC inhibitor SAHA-induced rapid-acting antidepressant behavior. We found that SAHA increases mRNA expression of CaMKIIβ, which in turn enhances the phosphorylation of AMPA receptor GluR1, resulting in increased trafficking of GluR1 in synaptic membrane in the hippocampus of mice treated with SAHA. Together, these results suggest CaMKIIβ-GluR1 signaling might be associated with SAHA-induced rapid-acting antidepressant behavior.

Report

(3 results)