| Project/Area Number |
17K07122
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | Tokyo Metropolitan Institute of Medical Science |
|---|
Principal Investigator |
UENO Kohei 公益財団法人東京都医学総合研究所, 脳・神経科学研究分野, 副参事研究員 (40332556)
|
|---|
| Project Period (FY) |
2017-04-01 – 2021-03-31
|
| Project Status |
Completed (Fiscal Year 2020)
|
| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | ドパミン / ショウジョウバエ / シナプス / 逆行性シグナル / Drosophila / dopamine / retrograde signal / ryanodine receptor |
|---|
| Outline of Final Research Achievements |
The dopaminergic neuron (DAN), which releases dopamine, has very large terminals. Thus, when the DAN is excited, it releases dopamine over a wide area of the brain. However, since memory formation requires neural circuit specificity , it was thought that DANs may also have local release mechanisms.
From the analysis of Drosophila isolated brains, I found that activated postsynaptic cells by odor and somatosensory inputs induce dopamine release from neighboring presynaptic terminals of DANs. By combining genetic and imaging analyses, I found that this phenomenon is achieved by a novel synaptic transmission mechanism in which carbon monoxide from the postsynaptic cells activates ryanodine receptors at the DAN terminal.
|
| Academic Significance and Societal Importance of the Research Achievements |
これまで、神経伝達物質の放出は、その伝達物質を放出する神経が興奮し、これによって神経終末のCa2+レベルが上昇することが唯一の機構であると考えられてきた。しかし、本研究において神経伝達物質の受け手である後シナプス細胞が活性化することが直接の引き金となりうること、さらに一部の終末だけで神経伝達物質を放出させることも可能であることを見出した。本研究成果はこれらの知見からシナプス伝達の新しい概念を提案するものである。
|
