2016 Fiscal Year Final Research Report
Mechanisms of gilal cell-dependent synapse remodeling in primary somatosensory cortex underlying development of chronic pain
| Project/Area Number |
26860380
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pain science
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| Research Institution | University of Yamanashi |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | アストロサイト / 神経障害性疼痛 / 一次体性感覚野 / ATP / シナプス再編 / 神経回路組み替え |
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| Outline of Final Research Achievements |
We showed that an increase in extracellular ATP concentration ([ATP]e) in S1 by PNI is an initial event that triggers the astrocyte-mediated mechanical allodynia. Using microdialysis screening in vivo, we found that 1) [ATP]e was increased within contralateral S1 by PNI, which was preceded by synapse-remodeling, 2) a single brief ATP-treatment into S1 was enough to induce excess Ca2+ excitation and up-regulation of thrombospondin-1 (TSP-1), one of synaptogenic factors, in astrocytes, synapse-remodeling in S1 and subsequent mechanical allodynia, and 3) the ATP-induced mechanical allodynia was dependent on astrocytic Ca2+ excitation. These results suggested that the increase in [ATP]e within S1 is a key event that initiates the astrocyte-dependent synapse-remodeling and subsequent mechanical allodynia.
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| Free Research Field |
神経薬理学
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