Regulation of synaptic plasticity via hetero-GPCR modulation: an analysis using surface plasmon resonance imaging

2017 Fiscal Year Final Research Report

• Project/Area Number: 26430012
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: University of Toyama
• Principal Investigator: Tabata Toshihide 富山大学, 大学院理工学研究部(工学), 教授 (80303270)
• Co-Investigator(Renkei-kenkyūsha): SHINOHARA Hiroaki 富山大学, 大学院理工学研究部(工学), 教授 (60178887) ; KAMIKUBO Yuji 順天堂大学, 医学部, 助教 (80509670)
• Research Collaborator: YOKOYAMA Tomoki ; FUKUSHIMA Toshiki
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: Gタンパク質共役型受受容体 / ニューロン / シナプス可塑性 / グルタミン酸 / ガンマ・アミノ酪酸 / Cキナーゼ

Outline of Final Research Achievements

In cerebellar Purkinje cells, type-1 metabotropic glutamate receptor (mGluR1), which serves as the trigger of synaptic plasticity underlying motor learning, is suggested to be complexed with adenosine A1 receptor (A1R) and B-type gamma-aminobutyric acid receptor (GABAbR). We applied surface plasmon resonance imaging and fluorometry to HEK-293 cells heterologously expressing these receptors and found that A1R and GABAbR can form complexes with mGluR1 and modulate mGluR1 signaling without the neuron-specific cellular environment. We also found that these modulations do not require Gi/o protein and may be induced dynamically with cerebrospinal fluid levels of adenosine and GABA. These findings provide an insight into the regulatory mechanism of cerebellar motor learning.

Free Research Field

神経生理学