Analysis of development of oligodendtocytes in autism-related mouse model
| Project/Area Number |
15K06753
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Nerve anatomy/Neuropathology
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
HORI Osamu 金沢大学, 医学系, 教授
TAKARADA Mika 金沢大学, 医学系, 助教
ISHII Hiroshi 金沢大学, 医学系, 助教
Higashida Haruhiro 金沢大学, 子どものこころの発達研究センター, 特任教授
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | グリア細胞 / アストロサイト / オリゴデンドロサイト / 自閉症スペクトラム障害 / 発達障害 / ミエリン / 大脳皮質 / 自閉症スペクトラム / 社会性 / 自閉症 / ギャップジャンクション / グリア / オキシトシン |
|---|
| Outline of Final Research Achievements |
The brain consists of neurons and glial cells. Recent research uncovers the importance of glial cells; their developmental abnormality causes various diseases such as autism spectrum disorders and aberrant cerebral cortex development. Herein, CD38 gene knocking-out is shown to cause aberrant development of glial cells, especially, those called astrocytes and oligodendrocytes. As CD38 knockout mouse exhibits abnormal social behavior, these abnormal glial development may be one of the reason for the abnormal behavior. The present study suggests the importance of glial cells for the cerebral cortex development and social behavior.
|
Report
(4 results)
Research Products
(25 results)
-
-
-
[Journal Article] CD38 positively regulates postnatal development of astrocytes cell-autonomously and oligodendrocytes non-cell-autonomously.2017
Author(s)
Hattori T, Kaji M, Ishii H, Jureepon R, Takarada-Iemata M, Ta HM, Le TM, Konno A, Hirai H, Shiraishi Y, Ozaki N, Yamamoto Y, Okamoto H, Yokoyama S, Higashida H, Kitao Y, Hori O.
-
Journal Title
Glia
Volume: 印刷中
Issue: 6
Pages: 974-989
DOI
Related Report
Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
-
[Journal Article] Atf6α deficiency suppresses microglial activation and ameliorates pathology of experimental autoimmune encephalomyelitis.2016
Author(s)
Ta HM, Le TM, Ishii H, Takarada-Iemata M, Hattori T, Hashida K, Yamamoto Y, Mori K, Takahashi R, Kitao Y, Hori O.
-
Journal Title
Journal of Neurochemistry
Volume: 139
Issue: 6
Pages: 1124-1137
DOI
Related Report
Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
-
[Journal Article] Deletion of Atf6α impairs astroglial activation and enhances neuronal death after brain ischemia in mice.2015
Author(s)
Yoshikawa A, KamideT, Hashida K, Ta HM, Inahata Y, Takarada-Iemata M, Hattori T, Mori K, Takahashi R, Matsuyama T, Hayashi Y, Kitao Y, Hori O
-
Journal Title
J Neurochem.
Volume: 132(3)
Issue: 3
Pages: 342-53
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
-
[Journal Article] DBZ Regulates Cortical Cell Positioning and Neurite Development by Sustaining the Anterograde Transport of Lis1 and DISC1 through Control of Ndel1 Dual-Phosphorylation2015
Author(s)
Okamoto M, Iguchi T, Hattori T, Matsuzaki S, Koyama Y, Taniguchi M, Komada M, Xie MJ, Yagi H, Shimizu S, Konishi Y, Omi M, Yoshimi T, Tachibana T, Fujieda S, Katayama T, Ito A, Hirotsune S, Tohyama M, Sato M.
-
Journal Title
J Neurosci.
Volume: 18;35(7)
Pages: 2942-58
Related Report
Peer Reviewed / Acknowledgement Compliant
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
