2007 Fiscal Year Final Research Report Summary
Studies of the mechanism generating left-right asymmetry of the brain
Project/Area Number |
16300101
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neuroscience in general
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Research Institution | Kyushu University |
Principal Investigator |
ITO Isao Kyushu University, Dept. Biology, Associate Professor (20183741)
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Project Period (FY) |
2004 – 2007
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Keywords | Brain / Left Brain Right Brain / Left-Right asymmetry of the Brain / Brain Asymmetry / Hippocampus / Neuronal circuitry / Synapse / NMDA receptor |
Research Abstract |
Left-right (L-R) asymmetry is a fundamental feature of higher-order neural function. However, the molecular basis of brain asymmetry remains unclear. We recently reported L-R asymmetry of hippocampal circuitry caused by differential allocation of N-methyl-D-aspartate receptor (NMDAR) subunit GluRε2 (NR2B) in hippocampal synapses (Science, 2003). Studies on ε1 (NR2A) knock-out (KO) mice. To investigate whether asymmetrical ε2 allocation is also related to the types of the postsynaptic cells, we compared postembedding immunogold labeling for ε2 in left and right Sch synapses on pyramidal cells and interneurons. To facilitate the detection of ε2 density difference, we used ε1 subunit KO mice, which have a simplified NMDA receptor subunit composition. We found that ε2 distribution was asymmetrical between left and right Sch-pyramidal cell but not Sch-interneuron synapses, indicating a postsynaptic cell-type dependent regulation of the asymmetry. Also, we found that, in ε1 subunit KO mice, the asymmetry of ε2 allocation results in left-right difference in NMDA receptor content and synaptic plasticity (J. Neurosci, 2005). Studies on iv mice. Iv is a spontaneous mouse mutant that possesses a mutation in the gene encoding the motor protein, Left-right dynein (Lrd). Fifty percent of iv/iv mice exhibit situs inversus, whereas the rest are normal (situs solitus). We found that the iv mouse hippocampus exhibited right isomerism of the synaptic distribution of the ε2 subunit. This laterality defect of the hippocampus is independent of the laterality of visceral organs. Therefore, the mechanisms responsible for the specification of L-R asymmetry differ between visceral organs and the brain (PLOS One, 2008).
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[Journal Article] Target-cell-specific Left-Right asymmetry of NMDA receptor content in Schaffer collateral synapses in ε1 knock-out mice2005
Author(s)
Y., Wu, R., Kawakami, Y., Shinohara, M., Fukaya, K., Sakimura, M., Mishina, M., Watanabe, I., Ito, R., Shigemoto
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Journal Title
J.Neuroscience 25(40)
Pages: 9213-9226
Description
「研究成果報告書概要(欧文)」より
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[Book] マウス脳の左右差
Author(s)
伊藤 功, 重本 隆一
Publisher
実験医学
Description
「研究成果報告書概要(和文)」より
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