2013 Fiscal Year Final Research Report
Glial conditioning mechanism through induction of development of neural circuit in cerebellar development
| Project/Area Number |
23500516
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | Toyohashi University of Technology |
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Principal Investigator |
YOSHIDA Sachiko 豊橋技術科学大学, 工学(系)研究科(研究院), 講師 (40222393)
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| Co-Investigator(Kenkyū-buntansha) |
HOZUMI Naohiro 豊橋技術科学大学, 国際協力センター, 教授 (30314090)
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| Co-Investigator(Renkei-kenkyūsha) |
FUKUDA Atsuo 浜松医科大学, 医学部, 教授 (50254272)
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| Project Period (FY) |
2011 – 2013
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| Keywords | GABA / プルキンエ細胞 / ATP / HDAC阻害剤 / 小脳発達 / 神経回路形成 |
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| Research Abstract |
We has developed the enzyme-linked transmitter photoassay device. Using this system, GABA release was observed in the immature cerebellar cultured glial cells without co-cultured neurons. Matured glial cells expressing GFAP released little GABA. This GABA release would relate to VGAT expression in glial cells. Stability of F-actin and plasmalemmal undercoat could be observed in the living cells using the acoustic microscopy. Valproate, general antiepileptic agent, hastened cerebellar development, especially the dendrite elongation of Purkinje cells. Valproate is known as the inhibitor of both GABA transaminase and HDAC. It is unknown which is primary factor, however, some HDAC inhibitors showed same effect. We developed the device for detection of released ATP relating synaptogenesis. In Valproate-treated animals, high ATP release was observed even in P6.
We suggested that GABA would be a conductor of cerebellar development, and HDAC inhibitors might disrupt it and hasten abnormally.
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Research Products
(49 results)
