Elucidation of activity-dependency and molecular mechanisms of synapse elimination
| Project/Area Number |
25830004
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurophysiology / General neuroscience
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
UESAKA Naofumi 東京大学, 医学(系)研究科(研究院), 助教 (70597624)
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | シナプス刈り込み / 小脳 / セマフォリン / Arc / 機能的神経回路形成 / スクリーニング / プルキンエ細胞 / 登上線維 / 逆行性シグナル / 神経活動 |
|---|
| Outline of Final Research Achievements |
In the present study, we have screened signaling molecules for synapse elimination in developing cerebellum during the period of elimination of redundant climbing fiber (CF) to Purkinje cell (PC) synapses, a representative case of synapse elimination in developing brain. We found that Arc mediates CF synapse elimination downstream of neural activity. In addition, two semaphorins, Sema3A and Sema7A, derived from postsynaptic PCs act as a synaptotoxin and a synaptotrophin, respectively, through their receptors on CFs. These findings have unraveled the long-unknown mechanism by which the information for eliminating or strengthening synapses is transmitted from postsynaptic cells to presynaptic cells. Our findings provide a new insight into the roles of semaphorins, a major family of intercellular signaling molecules known to play crucial roles in development of the nervous system, cell recognition in the immune system, and formation and regeneration of the bone.
|
Report
(3 results)
Research Products
(22 results)
