The functional analyses of Cbln-GluD1 signaling
Project/Area Number |
23500399
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neuroscience in general
|
Research Institution | Keio University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
SASAKI Tsukasa 東京大学, 大学院・教育学研究科, 教授 (50235256)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | デルタ型グルタミン酸受容体 / Cbln / AMPA受容体 / 海馬 / 小脳 / デルタグルタミン酸受容体 / トラフィッキング / 精神疾患 |
Research Abstract |
Although it was demonstrated that the delta2 glutamate receptor (GluD2) played crucial roles in synapse formation/maintenance and synaptic plasticity through interactions with Cbln1, function of GluD1 remains still elusive. Using GluD1-null mice, we investigated electrophysiological characteristics of the hippocampal CA1 neuron synapses in stratum lacunosum-moleculare where the entorhinal cortical neurons directly project. We found that GluD1 was critically involved in tuning NMDA/AMPA ratio and the threshold of synaptic plasticity. Furthermore, GluD1-null mice showed impairment in trace fear conditioning in which synaptic transmission in the stratum lacunosum-moleculare of the CA1 region is essential. It should be noted that this study, for the first time, revealed biological function of GluD1 in synaptic plasticity.
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Report
(4 results)
Research Products
(12 results)