Project/Area Number |
26430021
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurophysiology / General neuroscience
|
Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
Ono Katsuhiko 京都府立医科大学, 医学(系)研究科(研究院), 教授 (30152523)
|
Co-Investigator(Renkei-kenkyūsha) |
Takebayashi Hirohide 新潟大学, 大学院・医歯学総合研究科, 教授 (60353439)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | Olig2 / 視床 / 腹側視床 / 神経回路形成 / 軸索ガイダンス分子 / 転写因子 / 領域形成 / 視床隆起 / 大脳皮質 / Linx / 軸索ガイダンス / マイクロアレイ / in situ hybridization / 免疫組織化学染色 / マウス胎仔 / 背側視床 / 視床皮質投射 / 間脳 / prethalamus / 定量PCR / in situ hyubridization |
Outline of Final Research Achievements |
Thalamocortical axons (TCAs) extend from the dorsal thalamus to the cerebral cortex through ventral thalamus and ventral telencephalon. We aimed to examine how axons are regulated when they extend from the thalamus to the ventral telencephalon. Especially, we focused on instructive mechanisms in the ventral thalamus. For this purpose, we analyzed expression of axon guidance molecules in these areas. Candidate molecules were picked up from the microarray analysis of Olig2 deficient mouse forebrain which shows malformed TCA projection. Among the molecules that were shown to be altered their expression in the Olig2-KO mouse, qPCR elucidated that expression of some kinds of proteoglycan and that of Slit2 were really altered in the Olig2-KO mouse. However, in situ hybridization analysis showed no or few alteration in expression of these molecules. It is possible that subtle change of expression could alter axonal path finding.
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