| Project/Area Number |
24650194
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | University of Toyama (2013)
The University of Tokyo (2012) |
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Principal Investigator |
YOSHIDA Tomoyuki 富山大学, 大学院医学薬学研究部(医学), 准教授 (90372367)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | シナプス形成 / インターロイキン－１受容体 / インターロイキン-1 / インターロイキン１受容体 |
|---|
| Research Abstract |
Interleukin-1 receptor accessory protein (IL-1RAcP) is the essential component of receptor complexes mediating immune and inflammatory responses to interleukin-1 family cytokines. Using a fibroblast-neuron mixed culture assay, we found robust synaptogenic activity of IL-1RAcP in cultured cortical neurons. IL-1RAcP interacted with protein tyrosine phosphatase (PTP) delta through the extracellular domain. The synaptogenic activity of IL-1RAcP was diminished in cortical neurons from PTP delta knockout mice. Correspondingly, PTP delta required IL-1RAcP to induce postsynaptic differentiation. Furthermore, the spine densities of cortical and hippocampal pyramidal neurons were reduced in IL-1RAcP knockout mice. These results suggest that IL-1RAcP functions as trans-synaptic cell adhesion molecules in the brain and organize synapse formation through PTP delta .
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